EARLY SYMPTOMS (first few weeks of infection):
• Chronic sore throat (pharyngitis) that never fully heals (but many don’t get this).
• Constantly congested nose/sinuses/post nasal drip with unusually thick mucus.
ADDITIONAL SYMPTOMS (appear after a few months):
• Depression and low mood.
• Generalized anxiety disorder with very severe anxiety states (even bordering on psychosis).
• Powerful psychological changes and cognition disruptions.
• Loss of desires and sense of pleasure (anhedonia); loss of libido.
• Social withdrawal – escaping social activities more and more.
• Loss of drive and motivation (athymhormia).
• Memory problems both short-term and long-term recall.
• Unusual sleepiness and a tendency to fall asleep more.
• Chronic fatigue – notable loss of energy.
• Stomach aches and pains with stomach / bowel rumbling.
• Pins and needles (paresthesias), especially in the legs.
• Receding gums — a sudden onset of periodontitis, with brown plaque appearing on teeth.
LATER SYMPTOMS (appear at approximately 12 to 18 months):
• Slight wrinkling of the skin with unusual, fine-textured crêpe paper-like wrinkles.
• Weak legs and hips: legs and hip girdle feel loose.
• Weight gain, mainly on the belly (central obesity).
• Subtle loss of hearing acuity in identifying sounds.
• Progressive sensorineural hearing loss in the elderly.
• Emotional frailty, emotional lability, emotional flatness; irritability.
• Less frequently: tinnitus; blurred vision; occasional transient joint pains.
OTHER POSSIBLE SEQUELAE:
• Pericarditis, myocarditis and sudden heart attack in the previously healthy.
• Chronic, unrelenting systemic inflammation.
• Viral meningitis (can appear months after the initial infection).
This virus is also somewhat immunosuppressive, so secondary opportunistic infections may arise more frequently once someone has this chronic sore throat virus (especially in the first year or two of infection). This is a persistent virus, and once caught, the infection does not seem to resolve. It has been observed that this chronic sore throat virus gradually transmits from person-to-person through normal household contact, so once one person has it at home, most other household members will catch this virus within a year or so. Indeed, the above symptoms were not only observed in myself: various symptoms also manifested in 30 other people I know who caught this virus. This chronic sore throat virus is characterized by an unusually rapid incubation period: from point in time when you catch this virus (often through kissing an infected person), it takes a mere 12 hours approximately for the first sore throat or gastrointestinal symptoms to appear.
The more severe symptoms listed above appear in around 10% of people, but the majority of people contracting this chronic sore throat virus only seem to get much milder symptoms (as described here).
We will see below that this “chronic sore throat virus” is most probably an enterovirus of some type, such as a coxsackievirus B.
Here is my account of how I caught this chronic sore throat virus, and how it gradually began infecting my whole body.
This infection began with a bad sore throat that I caught. Being in excellent physical shape at that time, I thought nothing of it. I had no rash on my body, though the back of my throat and the rear arch of my soft palette were red and inflamed (see image), looking a bit like a herpangina sore throat, but without pain, blisters or ulcers. I paid little attention to it. Several weeks later, however, I noticed that my sore throat had not cleared up, and instead, the infection started spreading. This was strange, because I was very healthy at that point, HIV negative, with no previous medical problems, usually fighting off colds and infections very quickly. Yet this sore throat would not go away.
Within a month, this chronic sore throat virus had spread to my nose, which started producing unusually thick and heavy mucus. My nose and sinuses thus became blocked and stuffy, needing to be regularly cleared of this thick mucus every hour or two. (This thick nasal mucus congestion is now a permanent symptom). A constant stuffy nose like this is classified as chronic sinusitis, chronic rhinitis, post nasal drip, or rhinorrhea.
Then my lungs became infected, leading to a mild chest infection and a dry cough. Soon after this, the virus reached my stomach, which started aching a little and produced gas and bubbling sounds, which created some belching (my rumbling, aching stomach is also a permanent – but thankfully intermittent – symptom). The virus also spread to my intestines, where it also produced odorless intestinal gas (odorless flatulence), bowel rumbles and bowel bloating (now all permanent symptoms).
After another month, this viral infection manifested a distinct new phase: intense mental state changes suddenly appeared. These disturbing psychological symptoms started with a feeling of being very tense, anxious and uncomfortable, especially with people (even with friends and family). I became very weak mentally. My strength of mind rapidly disintegrated, and in particular, I became very frail and feeble emotionally. Other people seemed to perturb my mind, so it became quite unpleasant to socialize.
As a result of these psychological changes, I started avoiding social contact more and more, just because I found it a mental strain to be with people, even if they were good friends. Avoiding company made me lonely, yet being with people caused severe tension. This extreme anxiety made it impossible for me to continue to go to work, so I left my job.
Additionally, just reading or listening to facts and ideas created strong tensions in my mind, as I tried to process the information. So it seemed I could not cope with structured information very well either, even from a book, television or radio. This is more or less psychosis. As a coping strategy, I limited my time with people and information to help reduce this unpleasant mental tension.
Then I quickly became very apathetic. The apathy was towards all sorts of tasks and activities. My normal pro-active ‘can do’ attitude was replaced by a ‘not interested’ feeling – totally out of character. I am normally a motivated, enthusiastic and highly organized person. However, as this infection and its psychological effects progressed, I began to lose interest in the usual pleasures of life (a condition called anhedonia), including pleasure from sex. There was also a large loss of libido (loss of the desire for sex). Furthermore, much of my enthusiasm, drive and motivation just evaporated away (a condition called athymhormia).
I also began to experience some short-term memory difficulties, and inability to concentrate which caused problems in my day-to-day activities. There was some intelligence loss, particularly in my verbal, spelling and grammatical skills, and I found it a lot harder to recall words, names and other information from my long-term memory. Thus I found myself becoming less articulate, often mispronouncing words, and forgetting names.
Additionally, my physical body movements started getting a little more clumsy; I seemed to become physically less coordinated.
To sum up, psychologically, I became: anxious, depressed, avoiding social contact, unmotivated, emotionally delicate, confused, forgetful, clumsy, uncoordinated, with a dulled intellect, decreased verbal intelligence, and an impaired memory.
My virus also spread to friends and family (and then later to their friends and families), but quite slowly. For example, I would infect someone new only every month or two (just by normal household and social contact). That newly infected person would initially come down with the same herpangina-like sore throat symptom, and/or a gastrointestinal upset (gastroenteritis). Then, in most cases, they progressed to similar long-term symptoms, though usually not as severe as mine. Only around 1 in every 10 individuals seem get the more severe long-term symptoms. In certain people (but not in my case) infection with this virus caused uncharacteristic and irrational outbursts of sustained aggression to appear a few weeks after catching it. For most people catching this virus, there seems to be a delay of a few weeks to a month before the first psychological/neurological symptoms first begin to manifest.
(As an aside, these psychological symptoms make me wonder whether a virulent virus such as this one may be responsible for the apparent worldwide rise in autism, since its psychological manifestations relate to this condition. Certainly, a lot of previously normal people that caught this virus have reported that their “mind is definitely not functioning right”. And when this virus hits a whole family, sometimes, as a result of the mental changes, family members can become slightly more emotionally distant from each other, with family relations in general turning to a functional pragmatism. Some people with this virus start to avoid social contact a little, becoming less interested in other people. I noticed within my own mind that I lost the pleasure that normally arises from seeing friends, and from making new friendships. I think this loss of the ability to take pleasure in company is one reason this virus makes socializing less appealing. A second reason is the huge stress and mental tension this virus can cause, so you find you cannot relax in company. And a third reason is that, later on, irritability with people can become a very prominent mental symptom. All these factors disincline an individual from social activity.)
The next symptoms I experienced were more and more fatigue and sleepiness (hypersomnia). I seemed to fall asleep all the time, even when I was not that tired. Perhaps this virus has affected the area of the brain that controls sleep (the hypothalamus). As this sleepiness and fatigue progressed, I wondered if my condition could be classed as chronic fatigue syndrome (also called myalgic encephalomyelitis). A large loss of appetite appeared at this point also.
Four months after first catching this virus, a pins and needles or skin crawling sensation began to appear, first in my legs, but soon spreading to the rest of my body. There were constant sharp prickling sensations everywhere, which felt like they were located just beneath my skin. The severity of this prickling sensation varied from one day to the next. Sometimes the pins and needles would disappear for a week, but always return before long. These type of sensations are called paresthesias. Also at this stage, I noticed the onset of a very mild loss of sensation and loss of tactile sensitivity in the skin throughout my body.
The next set of symptoms to arise were a loss of smell (a condition known as anosmia). During some weeks my sense of smell would return a bit, but then the next week it would more or less disappear again. (It continued in these up-and-down cycles for two years. However, after several years, my olfactory capabilities have slowly improved, but have still not returned to anywhere near their original form.)
My oral health was then affected: my gums, previously extremely healthy and pink, began receding quite noticeably. Lots of brown plaque was suddenly deposited on my previously perfectly white teeth. No matter how much I brushed it away, the plaque still came back. Along with this increased plaque formation, and in spite of frequent tooth brushing, new dental caries (tooth decay/cavities) suddenly appeared. Previous to this, my oral health was excellent. Therefore, it seems I developed periodontitis (receding gums) from this virus within a matter of months.
This gum disease may be a manifestation of the immune-weakening effect this virus creates in the body, allowing bacteria to thrive and colonize the oral region. In addition, gum tissue can be directly attacked by connective tissue-dissolving enzymes created in viral infections (enzymes such as MMP-9).
Next, I noticed my vision began to deteriorate. So I had my eyes tested; there was nothing wrong with my eyes or my ophthalmic prescription. My vision seemed “muddy”, rather than optically blurred. For example, looking at say black text on a white page or screen, the letters are focussed, yet are slightly “smudged” and muddied by the white background.
About 12 to 18 months after first catching this virus, more strange symptoms manifested: a fine, crêpe paper-like wrinkling of the skin began appearing all over my body. This fine wrinkled skin first appears on the tops of the hands (see picture). The skin also shows a slight red, blotchy quality beneath its surface (but this is barely noticeable). I am guessing that this wrinkling is the result of collagen or elastin loss or damage under the skin, caused by the viral infection (again, probably due to connective tissue-dissolving enzymes). This wrinkling is not normal skin aging; it is definitely caused by the virus. The strange skin damage caused by this virus is usually only noticeable in people older than 30 or thereabouts. Even for people 30 to 50 say, this odd crêpe paper-like wrinkling is a relatively slight symptom. This virally-induced wrinkling manifested most prominently in people older than 50 (and very distinct from normal aging wrinkles). Searching through known dermatological conditions, the closest fit to my skin’s appearance I could find was a disease called mid-dermal elastolysis. More images of mid-dermal elastolysis can be found here.
Another symptom that manifested at this 12 to 18 month stage was weak legs and a loosening hip girdle. My pelvis-to-leg joints feel a little spongy and lacking in normal firmness. I suspect that the virus may be damaging the connective tissue in the ligaments of my pelvis, thus weakening the ligaments, and/or causing neuromuscular damage to the pelvic muscles. The result is a slightly less than sure walking gait, and a bit of a shuffling gait. This leg weakness and pelvic laxity is constant: it does not vary hour to hour, nor day to day. There is no loss of strength or spasm in the muscles either (except occasional cramps in my calf muscles). Differential diagnosis: in generalized anxiety disorder (GAD), weak legs are a common symptom, but a variable one. In GAD the legs are fine one minute, and the next they suddenly get weak and can almost give way, due to nervous system fluctuations. But my case is not like GAD: my leg weakness is constant, never varied. And not that weak.
Beginning at the 18 month stage, weight gain appears, mainly in the belly area (central obesity). Even in people who were previously athletically lean and muscular, this abdominal fat will appear. The deposition of abdominal fat can be caused by lowered growth hormone output from the pituitary gland, and/or the development of resistance to the hormone leptin; leptin resistance often arises in conditions of chronic inflammation.
After 2 or 3 years, an additional skin symptom appears: namely the color of the skin on the upper chest area becomes a little red/pink, and the skin texture in this area gets quite thick and oily (or waxy) in feel; the color of this upper chest rash is that of a heliotrope rash. In addition, new moles with a rough texture may appear on the skin; see this picture that I took of one the moles that appeared. These type of moles are called atypical moles, or dysplastic nevi.
This virus generally seems to cause immune system weakening, and this results in secondary opportunistic infections sometimes arising, for example: bad toothache, ear infections, eye styes, fungal skin infections, urinary-tract infections, etc (all requiring antibiotics or antimicrobials to clear). These opportunistic infections never appeared before contracting this virus. The highest immunosuppression occurs in the first few years of infection; after that, the immunosuppression seems to abate.
Furthermore, it seems that the virus itself, even years after first catching it, will occasional spontaneously cause an organ infection, such as the heart and its epithelial covering (acute pericarditis), and has spontaneously caused aseptic meningitis, years after first catching it. This virus appears to have a strong affinity for creating persistent infection of the mucous and serous membranes throughout the body.
Summary of viral characteristics: this virus is a systemic, respiratory, gastrointestinal and neurological virus, which persists chronically in the body, causes muscle weakening, chronic fatigue, and seems to have the ability to enter (or at least affect) the central nervous system, causing powerful and permanent mental state alterations such as mild memory problems, anhedonia, generalized anxiety disorder, and depression; it also seems to weaken the immune system, resulting in an increase of other opportunistic (eg: bacterial and fungal) infections. The virus has a very fast incubation period of around about 12 hours. This rapid incubation has been observed in several people when they initially caught this virus.
Other Symptoms: A whole cluster of other symptoms appear during the long course of this infection, including:
Progressive sensorineural hearing loss in older people (sensorineural hearing loss is the loss of the ability to hear low frequency sounds, typically in the range 125 Hz to 1000 Hz).
Subtle loss of hearing acuity is noticed in younger people, meaning that it becomes a little more difficult to identify environmental sounds, and interestingly, more difficult to sense their exact spatial location.
Tinnitus (high pitched sounds in the ears).
Sense of balance becoming noticeably less acute.
Dizziness spells (vertigo).
Chronic white tongue coating (called geographic tongue or migratory glossitis).
Glaucoma may appear after about 5 years.
Infection of the urethra
Viral headache lasting for several days.
Viral meningitis causing non-trivial and permanent changes in mental function.
Acute viral pericarditis
Acute viral myocarditis
Red heliotrope rash and waxy-textured skin on the chest just below the neck.
Cherry angiomas (tiny dark red pimples on the skin) amy appear after a few years.
New skin moles having a rough texture (called atypical moles, or dysplastic nevi) may appear after a few years.
Increased hair loss (alopecia).
Cold hands and feet — this very common symptom tends to appear a few years after initial infection. Likely due to poor blood circulation to the extremities, as a result of damage to the autonomic nervous system which controls the blood flow.
Dry mouth (Sjögren’s syndrome) — less saliva production.
Slow or non-healing wounds – small cuts sometimes not healing even after months.
Joint pains occasional transient joint pains (arthralgias), typically in only one joint.
Muscle cramps, especially in the calf muscles.
Lower back pain, due to strain or cramp in the lumbar region muscles.
Chronic systemic inflammation (requiring prolonged corticosteroids to control in one severe case).
Sharp stomach pains, which last for many hours, and often return every few days, are common (especially in the first year or two with this virus).
Flatulence — mild but permanent flatulence (which is odorless).
Tachycardia (sudden episodes of racing heart) and heart palpitations.
Slight numbness of the skin and loss of tactile sensitivity of the skin.
Static electricity buildup in the body (electric shocks) occurs as a sudden onset symptom in some people. These people start to experience strong static electricity discharge (electric shocks) when they touch earthed objects — a peculiar symptom. I speculate it may be related to changes in cellular ion channel function (ref: 1).
Reduced attention and concentration
Forgetting words and losing some of your vocabulary.
More difficulty in spelling words and remembering information all of a sudden.
Frequently selecting incorrect words while talking (and strangely, sometimes selecting a word which is incorrect, but from the same category as the right word – for example, saying “pun” when you meant to say “irony” – both are in the same category of literary devices).
Aversions to the smell and taste of certain foods (eg, meat) which were previously enjoyed.
Sound sensitivity may appear after a few years with this virus (this is where the brain finds it harder to cope with certain sounds and noises, such as screeching sounds, which seem to get “under the skin”). Such sensitivity to sounds is called hyperacusis.
More generally, a dislike of hectic environments, loud music, and overwhelming social ambiances appears after a few years with this virus.
Irritability towards people, circumstances, conversations, ideas — in other words, towards things in general — may occur.
Cognitive decline, reduced consciousness and perhaps mild dementia appear in certain individuals after around five years with this virus.
Emotional flatness/numbness — the brain’s emotional circuitry seems to get hit after a year or two with this viral infection, such that emotional responses become numbed (a condition known as “blunted affect”).
The above symptoms were observed in many people that caught this virus. Generally, I have only listed symptoms when at least two (and preferably more) people infected with this virus have manifested them; this is just to avoid the possibility of listing any co-incidental symptoms that may have appeared in infected people that are unconnected to this virus.
Certain individuals that are more severely affected by this virus can experience intense suicidal thoughts (suicidal ideation) every moment of every day, for several years, as if suicide is the only option that makes sense. These constant and harrowing suicidal thoughts are, I guess, a result of the high levels of anhedonia (complete loss of the capacity for joy and pleasure) and mental chaos induced by this virus. However even knowing that this suicidal mind state is caused by the virus does not help mitigate its piercing intensity. And although most people do not necessarily act on their suicidal ideations, the unrelenting presence of these thoughts shows just how profoundly this virus can disturb the normal brain chemistry of certain individuals it infects.
I found that taking SSRI antidepressant drugs (such as citalopram, escitalopram, fluoxetine, paroxetine, sertraline) greatly increases the intensity of these suicidal thoughts, within hours of first taking these drugs; so if you think you may have this virus, be very wary if you try SSRI antidepressants. Conversely, the powerful antidepressant drug imipramine was helpful for both my anhedonia and depression, and did not (at least in my case) amplify my suicidal ideations.
This virus appears to have precipitated several sudden heart attacks in my social group, and may have caused one fatal heart attack.
Note that this virus causes a long-term infection that is not cleared from the body, judging by the permanence of the symptoms it causes. Although some of its symptoms improve, other symptoms get worse over time. The mental state changes seem semi-permanent; the weak pelvic girdle and skin wrinkling seem to get a little worse over time.
As with many respiratory infections, once one person catches this virus, it will spread to most other members of their household. However, this happens slowly: it takes a year or more before everyone in the household catches this virus. So clearly the long-term contagiousness of this virus is moderately low. Nevertheless, in time, most of the household will have it, and will typically display either a chronically-congested nose (or sinus cavities) with thick, viscous mucus, or a chronic sore throat (or both), plus many of the psychological symptoms such as more fatigue, slight loss of short-term memory, slightly more social withdrawal, and some loss of motivation. The symptoms of weak legs and fine skin wrinkles tend to appear some time later. Generally, once an individual catches this virus, they are not quite themselves anymore. However, there is a range of individual responses to this virus: some people experience very disturbing and very distressing mental symptoms; others are more lucky, and their mental symptoms appear much milder. Only say 10% suffer the more severe mental symptoms and personality changes that I experienced; but everyone experiences some mental state change as a result of this virus (and these changes remain permanently). Approximately a third of the people who catch this virus get the chronic sore throat, and about two-thirds get a chronic production of thick nasal mucus. At best, this virus causes a noticeable lowering of the quality of life in people who catch it, but around 10% of people will suffer more severe problems.
None of the 10 or so medical professionals I saw were able to identify this disease or the pathogen causing it, but one infectious disease expert I communicated with said that, based on its symptoms, the pathogen I caught is very likely an enterovirus of some type, such as a Coxsackie B virus.
Certainly this infectious pathogen is probably a virus (rather than a bacterium, fungus or protozoan), based on the fact that three separate bacterial throat swab cultures my doctors conducted (one at a university hospital infectious disease center), showed negative results. Furthermore, stronger evidence that my pathogen is viral comes from its unusually rapid incubation period: the incubation period of my pathogen is around 12 hours; few bacteria can incubate this fast, and the bacterial species than can are easily detectable in a bacterial culture. Thus analysis of the incubation period suggests we are almost certainly dealing with a virus.
Should any readers have the same symptoms themselves and wish to share their experience and circumstances, please leave a comment. One purpose of this web site is to find people in a similar situation, and to share information and experiences. When posting a comment, you may want to make up an online name for yourself for anonymity purposes. No registration is required to post a comment, but filling out the email address field is a good idea, as when new information or treatments for this virus are found, I will send out details via email.
Note: there are many causes of chronic sore throat; so your chronic sore throat is unlikely to be caused by this virus, unless you have very similar symptoms. So for anyone with a sore throat for a few days: don’t panic, it is probably not this virus.
You may wish to go to the Treatments page, to see which supplements and drugs have proven beneficial in treating the symptoms of this virus. If you are suffering from the hellish constant anxiety symptoms that this virus seems to induce in certain people, the anti-anxiety treatments detailed have proved highly effective in treating these symptoms.
In the next section, we will explain why the virus described on this website is most likely an enterovirus, and might be a new strain of enterovirus.
DIAGNOSIS AND VIRAL IDENTIFICATION
In this section, we will determine what viruses are capable of causing my various symptoms, and attempt to identify which virus I have. Based on these manifested symptoms, we will also attempt to diagnose the specific disease conditions this virus has precipitated.
The most likely diagnosis for the main illness that I have developed from this virus is chronic fatigue syndrome (CFS), which is also called myalgic encephalomyelitis (ME), and often denoted as ME/CFS. However, ME/CFS is not the only disease condition this virus has precipitated, and it would seem that the diagnoses of peripheral neuropathy, chronic inflammation, anhedonic depression and anxiety disorder are appropriate descriptions for other groups symptoms this virus has caused.
How does chronic fatigue syndrome develop? Most common viruses, once you catch them, remain in your body for life – but usually in an inactive (or mostly inactive) state. However, in a small percentage of the population, these viruses may remain active (or partially active), and the infection continues indefinitely, but as a low level, “smoldering” infection. It is believed that this may lead to chronic fatigue syndrome. The full reasons why certain people are more susceptible to certain viruses are not known at this stage, but it is very likely that part of the susceptibility arises from the many microbes already living in a person’s body (if an individual’s existing viral load is already high, and they catch an additional virulent virus, their immune system may no longer be able to cope properly, and ME/CFS develops). Indeed, it has been frequently noted that people who were always a little bit frail in health (presumably due to the existing microbes in their system) are more likely to develop ME/CFS on contracting additional viruses.
Genetic factors are also known to be influential in who develops ME/CFS and who does not. Dr Jonathan Kerr has shown that 88 genes are abnormal in ME/CFS patients, many of these genes often relating to the function of the immune system. This may also help explain why certain minority of people have greater susceptibility to viruses and, on contracting a ME/CFS-causing virus, go on to develop ME/CFS.
Presumably another factor in who develops ME/CFS and who does not from a given virus is whether that virus is able invade the brain and central nervous system (CNS) of the individual, since the CNS is where the significant damage is done in ME/CFS. It may well be that those who do not get ME/CFS from a given virus have a more robust blood-brain barrier, and/or stronger cerebral immune system.
Around 0.2% to 2% of the population have chronic fatigue syndrome. Many people with severe cases of ME/CFS are bed-bound. Others with less severe chronic fatigue syndrome are able to keep working, but struggle considerably. Even people just mildly afflicted with one or more these viruses will probably perform less than 100%, both mentally and physically.
The reason I believe chronic fatigue syndrome is the correct diagnosis in my case is because nearly all my above-mentioned symptoms are classic ME/CFS symptoms. Thus the diagnosis of chronic fatigue syndrome generally fits. However, the unusual skin-wrinkling symptoms that people get from this virus are not normally found in ME/CFS, as far as I am aware (though another strange skin symptom can occur in ME/CFS patients: loss of fingerprints). Also, the extreme anxiety and anhedonia symptoms, which often are so bad they verge on mild psychosis, are quite unusual. This virus very suddenly causes these extreme mental state changes in certain susceptible people (perhaps in as much as 1 in 10 people who catch it).
It seems that this virus persists as a chronic infection, causing these ME/CFS symptoms; and it seems that there is a very high inflammatory response to this virus. It is this very strong inflammatory response, I believe, which causes these extreme mental states: in the brain, inflammation is known to cause significant mental symptoms such as anxiety, depression, anhedonia, etc.
To read more about chronic fatigue syndrome, and its causes and treatments, see the ME/CFS Info page.
Note also that many of the symptoms caused by this virus resemble peripheral neuropathy. Peripheral neuropathy is a disorder in which the body’s peripheral nervous system sustains damage. Symptoms of peripheral neuropathy may include: muscle weakness, muscle twitching, muscle cramps, walking gait abnormalities, blurred vision, slow processing of visual information (you see things with your eyes, but not with your brain), hearing loss, tinnitus, balance and coordination problems, dizziness or fainting, loss of smell, dry mouth, unusual sweating or inability to sweat normally (which may lead to heat intolerance), paresthesias, skin numbness, slow wound healing, bladder control changes, dysautonomia (autonomic dysfunction), cold hands and feet (from blood circulation problems), abnormalities in blood pressure or heart rate, postural orthostatic tachycardia syndrome (which is where you get a substantial increase in heart rate when suddenly moving from a seated to a standing position), and impotence in men (erectile dysfunction). The symptoms listed in this paragraph are those typically found in peripheral neuropathy; the symptoms highlighted in bold are the ones I experienced myself as result of this viral infection; thus it would seem that this virus does cause peripheral nerve damage, and it is clear that peripheral neuropathy is a good diagnosis for my symptoms.
This virus also seems to cause very mild chronic fatigue syndrome symptoms in nearly everyone that catches it. As this virus is not eliminated from the body, once you catch it, you will have this chronic infection and the disease conditions it precipitates for life. So I suspect this virus will have a significant impact on the mental and physical health of human populations as it begins to circulate more widely. It may take a decade or more before the majority of people have caught this respiratory virus, due to its relatively low contagiousness (see here for some epidemiological calculations for this virus). This virus will likely sneak in under the radar for many years, since the range of effects it can cause is wide: from heart attacks and periodontitis, to anhedonia and chronic fatigue syndrome.
Summary of Diagnosis
The virus described on this website appears to have caused a combination of diseases in me: chronic fatigue syndrome, peripheral neuropathy, chronic inflammation, anhedonic depression and anxiety disorder.
Identification: What Virus Might be Causing my Symptoms?
We will now look at the characteristic symptoms of a range of viruses, and see if any match my own symptoms. We must use some educated detective work to help identify the culprit virus. This is necessary because blood tests for active viral infections in the body, though helpful, often do not provide definitive conclusions, so there is no foolproof way of getting answers here. Infectious disease specialists will thus tend to look at the full clinical picture of a patient and, using all information possible, home in on the truth. So we will try to adopt this method as far as we can.
Unusually, I happen to know exact time I was exposed to this virus; so the fact that its first symptoms appeared 12 hours after this exposure, shows this virus has a very fast incubation period. This rapid incubation period was noted in many people who were infected by this virus (and an incubation period within 8 hours was actually observed in one particular person). This is an extremely fast incubation period, and should be of scientific note just in itself. Using this very valuable incubation period information, we can rule out a whole range of infectious microbial pathogens that have much longer incubation periods. Thus for example, the virus I caught could not possibly be Epstein-Barr virus (EBV), as EBV has an incubation period of 4 to 6 weeks, which considerably longer that the roughly 12 hour incubation period of my virus.
This fast incubation period, plus all the above listed symptoms of my virus can help identify it. Significant general characteristics of my virus are that it can cause a herpangina-like sore throat, with papules but no blisters or ulcers (so it is a respiratory virus), it can cause stomach and bowel symptoms (so it is a gastrointestinal virus), it can cause significant mental changes (so it is a neurological virus), it has mild immune-suppressive properties, it is communicable from person to person via saliva or nasal secretions, and it can cause chronic fatigue syndrome.
Given all this information, we will see in (the next section) that the virus I caught is possibly a Coxsackie B virus, or some other species of enterovirus.
However, be aware that other viruses can cause approximately similar symptoms. So if you have slightly different symptoms to me, one of the other viruses detailed below may be the culprit in your case.
Enteroviruses (Coxsackievirus B and Echovirus)
My Virus Precipitates Symptoms Typical of Enteroviruses
We here examine the fact that the symptoms produced by the virus described on this website strongly match the symptoms produced by enteroviruses.
Herpangina symptom: strong match. An initial characteristic symptom of my virus is a sore throat looking like herpangina (an inflamed red throat at the back of the soft palette). In my case, the herpangina was without any pain, and without blisters or ulcers, but with a cluster of small papules (raised pimples not producing pus) in the pharynx, these papules being a slightly whiter shade of the red/pink color of the throat itself. The name lymphonodular pharyngitis is given to a herpangina-type sore throat where there are only papules, but no blisters or ulcers; so lymphonodular pharyngitis may be a better description of my sore throat.
Herpangina sore throats are usually only caused by certain viruses of the Enterovirus genus, namely enterovirus 71, coxsackievirus A16, and coxsackievirus B species. Lymphonodular pharyngitis is normally caused by coxsackievirus A10 only (but this virus does not produce chronic infections, so we can rule this out). So regarding the herpangina (or lymphonodular pharyngitis) sore throat symptoms, we have strong match between the symptoms produced by my virus, and the symptoms that enteroviruses precipitate. (Note that more rarely, herpangina can be caused by echovirus (also from the Enterovirus genus), parechovirus 1, adenovirus, and herpes simplex virus; ref: 1.)
Incubation period: possible match. Figures quoted for coxsackievirus B incubation periods are 3 to 5 days, and echovirus incubation periods are 2 to 7 days. By contrast, the virus that I caught has a more rapid incubation period of around 12 hours (and I have noted my virus incubate in precisely 8 hours in one individual who caught it). So on first analysis, it might seem that the incubation period of my virus is too fast to make it a coxsackievirus B or echovirus. However, there are some enteroviruses than incubate in 12 hours, such as enterovirus 70, which is from the enterovirus D group. Interestingly enterovirus 68, another virus from the enterovirus D group, bears a strong relationship to rhinoviruses, and rhinoviruses (which are also in the enterovirus genus) have incubation periods of around 12 hours. I wonder whether a new recombinant enterovirus may have emerged, combining the genes of say coxsackievirus B with a more rapidly incubating enterovirus, such as those in enterovirus group D: such a recombination could explain why the incubation period of the virus described on this website is so remarkably fast.
Contagiousness: possible match. My virus is mildly contagious, and is transmitted from person-to-person via normal household or social contact, taking many months to a year before it transmits to everyone in the household. It will generally transmit when there is close contact such as kissing (especially French kissing), or when eating or drinking together (where spittle ejected from an infected person’s mouth may fall on another person’s food). The enteroviruses are generally easily passed from person-to-person via normal household contact, as they are spread by saliva and nasal secretions.
Organs and areas affected: strong match. Out of the various enteroviruses, a virus in the Coxsackie B group fits my symptoms particularly well, as coxsackievirus B often causes upper respiratory tract infection, gastrointestinal symptoms, significant neurological disease, persistent long-term infection, heart conditions, and systemic spread throughout the body — all of which have be precipitated by my virus. So regarding the organs and areas affected, we have strong match between the my virus, and enteroviruses. There are six serotypes within this coxsackievirus B group; these are coxsackievirus B1, B2, B3, B4, B5 and B6.
Immunosuppression: strong match. In terms of the immune system suppression symptoms I experienced: enteroviruses are known to cause immunosuppression, and one species of enterovirus, namely coxsackievirus B4, has been shown to attack the natural killer cells of the immune system (this might explain the immunodeficiency I observed, in that this disabling of natural killer cells can allow secondary opportunistic infections to arise more easily in an individual). So regarding the observed Immunosuppression symptoms, we have a strong match between the immunosuppression symptoms produced by my virus, and the immunosuppression symptoms enteroviruses are capable of producing.
Muscle weakness in pelvic girdle: strong match. How does enterovirus fit in with my virus’s symptom of muscle weakness in the pelvic girdle (that is, in the lower proximal muscles)? Well, proximal muscle weakness is the characteristic of the diseases of dermatomyositis and polymyositis, and these two chronic inflammatory myopathy diseases have been linked to group B coxsackieviruses (as well as parvovirus B19 infections, HIV and HTLV-I). Polymyositis generally affects the thighs and hips to begin with, but then progresses to all the proximal muscles (proximal muscles = the muscles in the central part of the body, from thighs to shoulders). So it is conceivable that the weakness in my lower proximal muscles might be explained by the action of an enterovirus.
Interestingly, lower proximal muscle weakness (hind limb weakness) was found in mice with polymyositis caused by the myopathic Tucson strain of coxsackievirus B1 (refs: 1, 2). Could this muscle-attacking stain of the coxsackievirus B1 (CVB1T) be the virus I caught? Polymyositis and dermatomyositis are diseases in which CD8 T cells attack the muscle tissue; in other words, these are autoimmune conditions, precipitated by viruses. Dermatomyositis is characterized by a heliotrope rash, a symptom myself and several other people with this virus display on the upper chest; along with my muscle weakness, my heliotrope rash therefore tends to support the idea that the virus described on this website is causing something akin to a mild, benign version dermatomyositis.
Hearing loss and increased tinnitus: strong match. Quite a few elderly people (aged 70+) that caught my virus soon (within year or so) experienced partial hearing loss, increased tinnitus, and sometimes even a mild loss of balance or dizzy spells. This little cluster of symptoms is actually a well-known syndrome called Meniere’s disease. Clinical investigation has shown that coxsackievirus B5, influenza B virus and varicella zoster virus are common causes of these type of ear symptoms. I myself noticed a loss in hearing acuity, after catching this virus. Greater age seems to predispose an individual to greater aural damage from this virus. So regarding the hearing loss and increased tinnitus symptoms, we have match between the symptoms produced by my virus and those produced by enteroviruses.
Chronic fatigue syndrome: strong match. What about the fact I developed chronic fatigue syndrome from my virus? Well enteroviruses, along with certain species of herpesviruses, are implicated as probable causes of chronic fatigue syndrome. So regarding the chronic fatigue syndrome precipitated by my virus, this strongly matches the characteristics of enterovirus.
Myocarditis, pericarditis and sudden heart attacks: strong match. In terms of the people who manifested myocarditis, pericarditis and sudden heart attacks after catching my virus, it is known that Coxsackie B virus is a very common cause of all these conditions. So regarding these cardiological events precipitated by my virus, these strongly match the characteristic diseases caused by enteroviruses such as Coxsackie B virus.
In conclusion: nearly all clinical signs and symptoms of my virus closely match those produced by enteroviruses, strongly suggesting that my virus is an enterovirus of some type. Dr John Chia (a highly regarded infectious disease specialist and expert in enterovirus and chronic fatigue syndrome) has very generously read my symptoms listed on this web site, and said my symptoms are consistent with a chronic enterovirus infection, and said that the other viruses listed below (like Epstein-Barr virus and HHV-6) do not really fit my symptoms. However these other microbes listed below can produce approximately similar symptoms, and are a useful reference for other people coming to this site who may have caught a different virus to mine.
There are a number of difficulties in testing for the presence of enteroviruses in the body in the case of chronic infections. This is because in chronic enterovirus infections, very few viral particles are present in the blood or tissues, and so only very sensitive laboratory tests are able to detect these infections.
ARUP Lab micro-neutralization tests are the only blood tests that are sensitive enough to be able to detect the very low levels of enterovirus antibodies typically found in chronic, long-term infections. If you suspect you may have the virus described on this website, these ARUP Lab micro-neutralization tests are probably the best ones to take.
Dr John Chia found that this ARUP Lab micro-neutralization antibody test is highly sensitive and specific: the test is able to detect the very small quantities of enterovirus antibodies that are present in the blood in chronic enterovirus infections, and furthermore, this test will determine which specific coxsackievirus B serotypes you have (it tests for all 6 Coxsackie B viruses), and which specific echovirus serotypes you have (out of the 5 echoviruses tested). These tests can be ordered directly from ARUP or ordered through Labcorp (if ordered through Labcorp, write on the form to specifically send this test to ARUP). The ARUP Lab coxsackievirus B1 to B6 antibody test is here, and the ARUP Lab echovirus antibody test is here.
The immunohistochemistry enterovirus test is a more sensitive (but unfortunately less specific) way of detecting chronic enterovirus infections. The immunohistochemistry test is more complicated, as it requires a tissue sample that must be collected from a stomach biopsy using an endoscope. The tissue sample is then tested for the presence of enterovirus VP1 protein. Dr John Chia has pioneered this approach for detecting chronic enterovirus infections in ME/CFS patients, and with this technique he has consistently demonstrated the presence enteroviruses in the stomach tissues of ME/CFS patients. This immunohistochemistry test can detect all types of enterovirus, and it is the most sensitive test of all, but it unfortunately does not determine the specific types of enteroviruses you have, whereas the ARUP micro-neutralization does determine the specific types of enterovirus you have.
Taking a enterovirus CFT test (Complement Fixation Test) for chronic enterovirus infection is NOT appropriate. The enterovirus CFT test is fine for testing acute enterovirus infections (in the first 10 days of infections), but it is of no use whatsoever for chronic enterovirus infections.
More details on the ARUP micro-neutralization test and the immunohistochemistry test can be found on the Enterovirus Foundation web site.
As explained, there is a good chance that the virus I caught as described on this site is an enterovirus, most likely a coxsackievirus B. Unfortunately, enteroviruses are very hard to treat, as there is not much in the way of effective antiviral drugs for enterovirus infections.
Intravenous interferon therapy can fight off an enterovirus infection in ME/CFS patients, but the virus and its symptoms generally return within six months or so (and interferon costs around $5000 per course of treatment).
The drugs ribavirin (antiviral drug), arbidol (antiviral drug), amiloride (diuretic drug), fluoxetine (antidepressant drug Prozac) and acyclovir (or valacyclovir) have some benefit against coxsackievirus B infection.
I have tried several of these drugs, but I did not have great success, at least for the short time periods of around a month that I tested them for.
Selenium 400 mcg daily on an empty stomach and vitamin E 400 IU daily are recommended, as deficiency in either of these nutrients leads to increased virulence of coxsackievirus B. In particular, I find selenium supplementation seems to combat the fatigue produced by this virus. It takes about a week of daily selenium supplementation before you notice increased energy.
Latent herpes family virus infections in the body may reactivate as a result of the immunosuppressive action of the virus described on this website, and may therefore be contributing to the overall symptoms. These herpes family viruses are treatable to a degree with drugs such as valacyclovir (Valtrex) 500 mg to 1000 mg twice daily or famciclovir (Famvir) 250 mg to 500 mg twice daily.
Dr John Chia (an infectious disease clinician and expert in enterovirus infections) has had some success using a herbal extract of Sophora root called oxymatrine for his patients with ME/CFS and chronic enterovirus infections: around 25% of people find oxymatrine works well for them. Relapses in symptoms can occur on discontinuation of oxymatrine. The dose is one oxymatrine 300 mg tablet, taken 1 to 3 times a day (start with 300 mg daily, and over the weeks, slowly increase to 3 x 300 mg tablets daily).
I tried oxymatrine for this virus, but in my case, it did not help. However it is worth trying oxymatrine for a few months to test it.
There are several other herbal supplements that have mild efficacy against coxsackievirus B, as follows:
Terminalia chebula (haritaki, He Zi) • Emblica officinalis (Phyllanthus emblica, amla) root • Trichosanthes root (Tian Hua Fen) • Rhodiola rosea (golden root) • curcumin • emodin (from Japanese knotweed) • Astragalus membranaceus • Spatholobus suberectus Dunn (Ji Xue Teng) • ursolic acid (found in basil essential oil) • Bupleurum kaoi (Chai Hu) • Glycine max (black soybean extract, Dan Dou Chi) • DHEA (dehydroepiandrosterone) • sodium selenite (a form of selenium) • EGCG (an extract from green tea) • Epimedium (horny goat weed) • baicalein (found in Scutellaria baicalensis) • nicotinamide (aka: niacinamide, a form of vitamin B3) • acemannan (aloe polymannose from aloe vera leaves) • Aegle marmelos Corr (bael fruit powder, bilva powder) • Azadirachta indica (neem) • hinokitiol (found in hiba oil) • Sophora flavescens root (Ku Shen) • Isatis tinctoria (dyer’s woad, Da Qing Ye, Ban Lan Gen).
I did not have much success with these herbal supplement antivirals, at least for the short time periods of around a month that I tested them for.
References for the antiviral efficacies of the above supplements and drugs can be found on the Treatments page.
Part of the difficulty in treating a chronic enterovirus infection is that this virus can exist in two distinct forms in the body: the regular enterovirus form, and the non-cytopathic enterovirus form. The infection begins with the normal regular enterovirus, but then some of these regular enteroviruses actually turn into non-cytopathic enteroviruses within the body. Whereas regular enteroviruses do not remain inside a human cell for long (they just enter a cell, replicate themselves, kill the host cell though lysis, and then wander off to infect more cells), by contrast non-cytopathic enteroviruses live within human cells on a long term basis, and do not kill the cell they live in.
Non-cytopathic enteroviruses do not have an outer shell (called a capsid) to protect themselves, and non-cytopathic enteroviruses cannot break out of human cells by lysis and then travel to infect more cells. You can think of a regular enterovirus as a snail with its shell, and a non-cytopathic enterovirus as a snail that has lost its shell and cannot replace it.
However, there is some evidence to suggest that non-cytopathic enteroviruses may be able to jump into and infect adjacent cells: this study demonstrates that a coxsackievirus B seems to be able to induce cellular protrusions (tentacle-like arms) to grow out the cell it lives in, and these protrusions may act as a cell-to-cell tunnel that allows non-cytopathic viruses to move into and infect new cells in close proximity; there is actually a time-lapse video of these coxsackievirus B-induced cellular protrusions that you can watch (see file 1 in the study’s supplemental material).
Many antivirals will target the regular enteroviruses, but unfortunately they do not touch the non-cytopathic enteroviruses that live inside human cells. These non-cytopathic enteroviruses are not detected by any standard laboratory tests either.
Non-cytopathic enteroviruses are also called by other names, including non-cytolytic enteroviruses, defective enteroviruses, and terminally-deleted enteroviruses.
Newly Emerging Enteroviruses
Let us look at some newly emerging enteroviruses, as these might be candidates for the identity of the virus I caught.
The Centers for Disease Control note that there may be a new more virulent strain of Coxsackie B1 virus in circulation. This is because there has been an increased level of coxsackievirus B1 infections in the United States, and these Coxsackie B1 infections have sometimes caused severe neonatal disease, as well as five baby deaths in 2007. Normally Coxsackie B infection is not fatal, so this more virulent killer Coxsackie B1 virus is clearly something nasty. Could this killer Coxsackie B1 virus be the cause of my symptoms?
Another possible candidate for my virus is the virulent new FY-19 strain of coxsackievirus B3 identified in China in 2008. This CVB3 seems to exhibit an unusually rapid incubation period – as has been consistently observed in the virus described on this website.
Several other new enteroviruses have also been discovered in the last decade: enterovirus 75 was found in Spain and circulating in Europe, and is associated with viral (aseptic) meningitis; enterovirus 93 and enterovirus 94 were found in the Congo and are associated with acute flaccid paralysis; enterovirus 104 was found in Switzerland and is associated with respiratory tract infections, otitis media (ear infection) and possibly brain and central nervous system infection; enterovirus 109 was identified from an outbreak of acute pediatric respiratory illness in Nicaragua, but the symptoms of EV-109 are not fully known. Thirteen other new enteroviruses (EV79–88, EV97, and EV100–101) were also identified this last decade using molecular identification methods. For more details of newly emerging enteroviruses and enterovirus outbreaks, see the Emerging Viruses page.
In the next sections, we look at other viruses, bacteria and parasites that can cause symptoms roughly like those I experienced, and which may also cause chronic fatigue syndrome. But to re-iterate: these viruses below are NOT good candidates for my virus’s identity; my virus is most likey an enterovirus.
Human Herpes Six Virus
Human herpes 6 virus (HHV-6), especially the more severe A-variant, called HHV-6A, can induce immunodeficiency, neurological symptoms and chronic fatigue syndrome. HHV-6A inhibits immune function by blocking the growth of dendritic cells and interleukin-12 production. There has been some speculation that HHV-6A is partly responsible for the immune deficiency found in HIV/AIDS. Dr. Robert Gallo, the co-discoverer of the HIV virus, believes that in tandem with HIV, HHV-6A accelerates the development of AIDS.
So could I have caught a virulent strain of HHV-6? Again, unlikely in my case, since the incubation period for HHV-6B is 5 to 15 days, whereas my virus has an incubation period of around 12 hours. (The incubation period for HHV-6A is not really known, but it may be similar to that of HHV-6B.)
Over 90 percent of the US population have HHV-6B in their bodies (but mostly in a latent, inactive state). The more severe HHV-6A variant is found in probably less than 3 percent of the US population. An active HHV-6 infection can cause chronic fatigue syndrome symptoms. Testing for an active HHV-6 infection is straightforward, and can be done by a blood antibody test. However, most lab tests for HHV-6 cannot distinguish between the nasty A-variant and the more benign B-variant of the HHV-6 virus. One test that can distinguish HHV-6A from HHV-6B is the nested PCR, and is available here: HHV-6A testing. More info on HHV-6A testing can be found here: 1, 2, 3.
For chronic fatigue syndrome due to HHV-6, treatment success has recently been achieved using the antiviral drug valganciclovir. The drug Nexavir (formerly Kutapressin) has also been helpful for patients with chronic fatigue syndrome caused by the human herpes six virus. The anti-malaria drug artesunate has significant efficacy against HHV-6.
Supplements for HHV-6
The herb artemisinin may have some efficacy against HHV-6, but because artemisinin has poor bioavailability, you will get better results from taking the drug derivative of artemisinin: artesunate, as mentioned in the paragraph above.
Parvovirus B19 is known to cause a persistent bodily infection as well as connective tissue disease. It is a frequent cause of chronic fatigue syndrome symptoms. Parvovirus B19 can also cause carpal tunnel syndrome, rheumatoid arthritis, vasculitis, Raynaud’s disease and anemia. In my case, parvovirus B19 can be ruled out, as its incubation period is 4 to 14 days, whereas my virus has a faster incubation period of around 12 hours.
Parvovirus B19 Testing
By adulthood, 50% of the US population have parvovirus B19 in their system. Testing to see if you have an active Parvovirus B19 infection is very straightforward, and can be done with a blood test.
Parvovirus B19 Treatments
For chronic fatigue syndrome caused by parvovirus B19, intravenous immunoglobulin (IVIG) treatment has worked in some cases.
Epstein-Barr virus (EBV), also called HHV-4, is a member of the herpes family. Most people know Epstein-Barr as the virus that causes mononucleosis. However, EBV has long been suspected in playing a causal role in chronic fatigue syndrome. This herpes virus can create an immunocompromised state in an individual.
Epstein-Barr virus (and cytomegalovirus also) is implicated in the oral health condition periodontitis, in which the gums are inflamed and receding (I fast developed periodontitis from the virus I caught). Periodontitis gum disease is in part due to proliferating oral bacteria; I assume that my oral bacteria are multiplying as a result of a slight immunodeficiency. Periodontitis is also associated with connective tissue dissolving enzymes (which we address later). Incidentally, gingivitis, which is where the gums are inflamed, but not receding, is associated with herpes simplex and varicella-zoster viruses. However, I have the more severe dental condition of periodontitis, not gingivitis.
Epstein-Barr can produce significant neurological symptoms. Thus this virus does fit many of my symptoms. So could I have a virulent strain of Epstein-Barr virus? One difficulty with this hypothesis is that the incubation period of EBV is 4 to 6 weeks, whereas my virus incubates in around 12 hours.
In most cases, active Epstein-Barr virus infections that cause chronic fatigue symptoms do not persist for more than around 4 months, and chronic EBV infection is rare. Research mostly indicates that Epstein-Barr virus is not connected to chronic fatigue syndrome, though partial reactivation of latent EBV may contribute to ME/CFS symptoms.
Around 95% of the world population have the Epstein-Barr virus in their bodies (in a mostly latent state), but most people do not suffer any extreme symptoms because of this. However, if you have an active long-term Epstein-Barr virus infection, this may cause chronic fatigue symptoms. Testing to see if you have an active Epstein-Barr virus infection is very straightforward, and can be done with a blood test that detects EBV antibodies.
In terms of treatments for chronic fatigue caused by Epstein-Barr, the antiviral drugs valacyclovir (Valtrex) and acyclovir (Zovirax) can be effective for treating chronic fatigue caused by Epstein-Barr virus. These drugs have a very good safety profile.
The drug Nexavir (formerly Kutapressin) has been helpful for patients with chronic fatigue caused by Epstein-Barr virus. Dr Kenny de Meirleir at Red Labs (located in Belgium and the USA) uses Nexavir. Dr Derek Enlander (located in New York) also uses Nexavir. Dr Paul Cheney uses artesunate in his treatment protocol for Epstein-Barr virus (and for HHV-6 virus).
Supplements for Epstein-Barr
The following supplements have a useful anti-EBV effect: turmeric, passionflower and sesame seed oil – these inhibit the Epstein-Barr virus (ref: 1). Other anti-EBV supplements include: lysine, ginger, licorice, curcumin, EGCG (from green tea), red marine algae, cayaponia tayuya root, pau d’arco herb, beetroot extract (Beta vulgaris), olive leaf extract, lemon balm (Melissa officinalis), citrus flavonoids, andrographis paniculata.
Other Chronic Fatigue Syndrome Viruses
Cytomegalovirus is another virus that can create chronic fatigue syndrome symptoms. Cytomegalovirus (CMV) can pass from person-to-person via saliva (as well as via urine, semen, cervical secretions, blood, and breast milk). However, cytomegalovirus has a fairly long incubation period of 4 to 12 weeks. Since my virus has an incubation time of around 12 hours, we can safely rule out the possibility that my virus is the cytomegalovirus.
Up to 20% of US children are infected with cytomegalovirus before they reach puberty, and more than 50% of the US adult population have cytomegalovirus in their bodies. Note that cytomegalovirus is often an opportunistic virus: if you have cytomegalovirus lurking your system already, although the immune system keeps it in check normally, the immune-suppressing actions of other viruses or bacteria may allow any latent cytomegalovirus in your body to re-activate and start causing trouble. Drug treatments for cytomegalovirus include: aspirin, artesunate, ganciclovir and foscarnet. Supplement treatments for cytomegalovirus include: artemisinin, chlorella, clove, Terminalia chebula, baicalein, genistein, ginger, hypericin, monolaurin, lactoferrin.
Varicella zoster virus (the virus which causes chickenpox) may be linked to chronic fatigue syndrome: this paper hypothesizes that at least some cases of chronic fatigue syndrome are caused by the reactivation of varicella zoster virus (or other herpes viruses) in the peripheral nerve ganglia.
Neurovirulent Influenza A virus attacks brain regions such as the substantia nigra (a brain area linked to motivation), the habenular, thalamus, hypothalamus and the brainstem. There are 10 human serotypes of influenza A, including: avian influenza (bird flu) H5N1, which may cause a human pandemic in the future; and swine influenza H1N1, which has infected the human population already. Influenza has an incubation period in the range of 1 to 7 days, but is typically 2 to 3 days. Influenza A infection can be treated with the neuraminidase inhibitors listed above; the herb asafoetida has efficacy against influenza A virus.
Herpes simplex virus I and II may be contributory factors in ME/CFS (it has been noted that more ME/CFS patients have antibodies to both HSV-1 and HSV-2 than do controls). Drug treatments for herpes simplex virus include: valacyclovir, acyclovir, heparin. Supplement treatments for herpes simplex virus include: creatine, lysine, lithium, clove (eugenol extract), curcumin, Lobelia chinensis, propolis, lactoferrin, Centella asiatica (gotu kola), licorice.
The viruses HHV-7, hepatitis C, and HTLV I & II have also been singled out as casual or contributory agents in ME/CFS.
Ross River virus, a mosquito-borne virus found in parts of Australia and other countries, has been associated with chronic fatigue syndrome (though most infections of Ross River virus in humans do not produce clinical symptoms and go unnoticed).
XMRV, a gamma retrovirus, was found in ME/CFS patients by Dr Judy Mikovits at the Whittemore-Peterson Institute (WPI). However, other researchers have so far been unable to replicate these findings.
JHK virus, a retrovirus discovered by Dr Sidney Grossberg was found in ME/CFS patients. Dr Elaine Defreitas found a HTLV-II-like virus in ME/CFS patients.
Then there is Borna disease virus (BDV) to consider. The Borna disease virus can cause depression and anhedonia (though the thorough work of Dr Ian Lipkin found no link between bornavirus and chronic fatigue syndrome). About 1 in 3 people in the general population are found to have antibodies to bornavirus. Bornavirus is generally thought to be a zoonotic virus (one contracted from animals) that does not pass from person-to-person, or if it does, its transmission is only very minimal. By contrast, the virus I caught transmits quite easily from human-to-human.
Bacterial Causes of Chronic Fatigue Syndrome
Bacteria such as Chlamydia pneumoniae and Coxiella burnetii (which causes Q fever) are responsible for some cases of chronic fatigue syndrome. These bacteria can be treated with antibiotics. The incubation period of Chlamydia pneumoniae is around 3 to 4 weeks; the incubation period of Coxiella burnetii 2 to 3 weeks; these incubation periods are too slow to be my pathogen, which has a much faster incubation period of around 12 hours.
Brucella bacteria may also cause chronic fatigue syndrome-like symptoms. This bacterium can be treated with antibiotics. Brucella’s incubation period is 1 to 3 weeks.
Mycoplasma species bacteria such as Mycoplasma fermentans, Mycoplasma hominis and Mycoplasma penetrans are sometimes found at higher levels in ME/CFS patients than in healthy people, and it has been speculated that Mycoplasma species may contribute to ME/CFS symptoms.
Protozoal Causes of Chronic Fatigue Syndrome
Giardia lamblia, a protozoan parasite that infects the small intestine causing giardiasis, has been shown to later lead to ME/CFS in a small percentage (around 5%) of individuals infected with it.
Toxoplasma gondii (a protozoan parasite found in cat feces and undercooked meat) has been known to cause pronged fatigue.
Other ME/CFS Causal, Contributory or Predisposing Factors
Why do some people, when they catch the virus described on this website (or some other ME/CFS-associated virus), develop chronic fatigue syndrome, while others do not (even though the other may get a very mild version of ME/CFS)? This discrepancy may be explained by predisposing factors, which increase the risk of developing ME/CFS. Some predisposing factors for acquiring ME/CFS are as follows.
Exposure to organophosphate pesticides has been implicated as a causal, contributory or predisposing factor to ME/CFS. Exposure to significant quantities of mold toxins (usually from water-damaged buildings) is a causal, contributory or predisposing factor for precipitating ME/CFS (certain species of mold contain potent neurotoxins). Exposure to ciguatoxin can result in chronic fatigue syndrome. Exposure to ionizing radiation is a cause of ME/CFS-like symptoms (post-radiation syndrome). Chronic fatigue syndrome can sometimes ensue after an episode of meningitis. Chronic fatigue syndrome can very occasionally appear after having major surgery. Sometimes a major physical trauma — particularly a motor vehicle accident – can precipitate ME/CFS. Food poisoning very occasionally leads to ME/CFS. Chronic fatigue syndrome has sometimes been precipitated by hepatitis B virus vaccination, but this is rare. Silicone used for breast and other implants, as well as silicone injections, can in rare cases cause an ME/CFS-like illness, as well as autoimmune conditions. Exposure to tung oil has been proposed as a cause for ME/CFS.
Already having the conditions of: irritable bowel syndrome, interstitial cystitis, and/or recurrent urinary tract infection may act as predisposing factors to acquiring ME/CFS. It may well be that these conditions are caused by microbes, thus already putting strain on the immune system; then, when a person contracts a further microbial agent such as the virus described on this website, the immune system can no longer cope (or develops some pathologies itself), and as a result, chronic fatigue syndrome ensues.
Hidden infections in the body, such as dental infections in root canals, or bone infections, may cause chronic fatigue syndrome, or ME/CFS-like symptoms (but this is very rare). Bacteria in such local hidden infections can produce toxins that cause system wide problems (see focal infection theory).
Leaky gut syndrome (intestinal permeability) may also be a contributory or predisposing factor to ME/CFS. A leaky gut may allow lipopolysaccharide (LPS), a molecule originating from Gram-negative bacteria the gut, to escape from the gut into the blood stream, where this LPS will cause a potent inflammatory response (the immune system is designed to mount a very high inflammatory response on encountering LPS, as it assumes this means there are Gram-negative bacteria about).
Other co-morbid conditions often seen to accompany (or arise after acquiring) chronic fatigue syndrome include: multiple chemical sensitivity (increased allergies), temporomandibular joint disorder (problems with the jaw joint or jaw muscles), myofascial pain syndrome, attention deficit hyperactivity disorder, eating disorders, chronic headaches / migraines, endometriosis, chronic pelvic pain syndrome (prostatitis), Hashimoto’s thyroiditis, prolapsed mitral valve, Raynaud’s disease, and Sjögren’s syndrome (sicca syndrome).
An Emerging New Respiratory Virus?
In the last decade or two, many new human respiratory viruses have been discovered. These include: human metapneumovirus virus (hMPV), mimivirus (in the Mimivirus genus), parvovirus 4, parvovirus 5, human bocavirus (in the Parvovirus genus), WU virus and KI virus (in the Polyomaviridae family), Torque teno virus (TT virus), melaka virus (in the Reovirus genus), mapuera virus and menangle virus, New Haven or NL63 coronavirus, coronavirus HKU1, titi-monkey adenovirus (TMAdV adenovirus). New viruses that infect humans have been found across seven genera in the Picornaviridae family: enterovirus 75, enterovirus 93, enterovirus 94, enterovirus 109 (in the Enterovirus genus), Ljungan virus (in the Parechovirus genus), Saffold virus (in the Cardiovirus genus), Aichi virus (in the Kobuvirus genus), cosavirus A to D (in the proposed new Cosavirus genus), klassevirus 1 (in the proposed new Klassevirus genus) and Seneca Valley virus (in the Senecavirus genus). The clinical signs, symptoms and pathogenesis for most of these viruses are not fully known at this stage. Could my virus be an emerging infectious disease within this list, or an as yet unknown and unnamed emerging viral pathogen?
Notes on These Newly Discovered Viruses
Viruses from the Cardiovirus genus cause serious disease, mainly in rodents, including diabetes, myocarditis, encephalomyelitis, and multiple sclerosis-like disseminated encephalomyelitis. Saffold virus is a particular Cardiovirus that can infect humans. Currently 9 Saffold virus types have been discovered (SAFV-1 to 9). Studies on SAFV-3 show that it is a very common virus, found in more than 90% of older children and adults.
Melaka virus symptoms are very similar to that of flu infections: fever, cough and sore throat. Torque teno virus is ubiquitous: found in more than 90% of adults worldwide, but human pathogenicity has not yet been established. Human metapneumovirus is ubiquitous: there is almost 100% seropositivity for hMPV antibodies in adults.
The virus described on this website has low prevalence in the general population (see here for how this is known). Thus newly discovered viruses like SAFV-3, TT virus and hMPV, which are very prevalent, cannot possibly be candidates for virus described on this website.
Diseases With Similar Symptoms: Differential Diagnoses
The set of symptoms that this virus precipitated in me primarily resembles chronic fatigue syndrome (ME/CFS), (though it is not entirely clear that this is ME/CFS). There is considerable symptom overlap between ME/CFS and these following diseases: lupus erythematosus, Lyme disease, chronic hepatitis C virus infection, celiac disease, hypothyroidism and anemia, and these conditions should first be tested for and ruled out before you consider a diagnosis of chronic fatigue syndrome. Please also see this list of diseases that have symptoms very similar to ME/CFS.
To help distinguish which of the above diseases you may have, a differential diagnosis is very useful. A differential diagnosis is a set of rules that are used to distinguish between two diseases that have very similar symptoms. A differential diagnosis works like this: when two diseases have nearly the all same symptoms, there will nevertheless generally be a few particular symptoms or laboratory test results that are present in one of the diseases, but not the other. A differential diagnosis focuses on these particular unique symptoms and test results, in order to determine which of the two diseases you actually have.
The following differential diagnoses can aid in distinguishing the ME/CFS-like symptoms of this virus from other conditions:
Lupus differential diagnosis: Systemic lupus erythematosus versus the virus described on this website:
• A red butterfly rash on the face is a characteristic symptom of lupus, but my virus has not precipitated this symptom in anyone. Skin rashes most commonly develop on the face, wrists and hands in lupus, but by contrast my virus tends to cause a mild heliotrope rash on the chest.
• Join pain is common in lupus (sometimes with intermittent joint swelling too), but these are not really symptoms produced my virus (my virus may cause very occasional transient joint pain in some people, lasting a few days, and typically only in one joint).
• Lupus is not contagious, whereas my virus is mildly contagious by normal social contact.
Lyme disease differential diagnosis: Lyme disease (Borrelia burgdorferi infection) versus the virus described on this website:
• A herpangina-like sore throat appears at the start of the infection with my virus in around one third of all cases; Borrelia burgdorferi does not cause a herpangina-like sore throat.
• Muscle laxity, primarily in the pelvis, can be caused by my virus. Borrelia burgdorferi in fact often produce the opposite: muscle stiffness, especially in the neck.
• Chills (uncontrolled shivering symptoms) often manifest in Lyme disease, but there are no such symptoms with my virus.
• Painful joint aches are frequently found in Lyme disease, but my virus does not really cause these (my virus may cause very occasional transient joint pain).
• My virus is mildly contagious by normal social contact (many people catch this virus from kissing on a date — with its first symptoms rapidly appearing 8 to 24 hours later). My virus will generally slowly spread to every member of your household, and all of your friends. By contrast, Borrelia burgdorferi is not contagious (although there are some rare, unproven anecdotal reports of Borrelia burgdorferi transmitting through sex, Borrelia burgdorferi certainly do not spread by kissing and normal social contact as my virus does reasonably easily).
CLINICAL SIGNS AND SYMPTOMS
In this section we provide a categorial summary of the clinical signs and symptoms of the virus described on this website, in order to help characterize the virus. These signs and symptoms were collated through careful observations on myself, and on 30+ other people in my social group who also caught this same virus. This set of 30+ people observed includes all ages, both sexes, and also different nationalities.
Mode of Transmission
The mode of transmission is the means by which an infectious microbe first enters the body (for example: by saliva, by blood, or by insect bite). It is clear that the virus described on this website is transmitted person-to-person via saliva and/or nasal secretions, and that this virus can transmit during close social contact. Furthermore, once one member of a household or workplace is infected with this virus, it has been noted that pretty much all of the other members will catch the virus from them within a year or so. The fact that transmission is not that fast (compared to a cold or influenza virus for example) suggests that not that many viral particles are shed by an infected individual, and/or that these shed viral particles do not survive long in the environment. It has been observed that transmission of this virus often occurs through intimate kissing, and also when sharing food or drinks on the same table (where spittle ejected from an infected person’s mouth may fall on another person’s food).
The incubation period is the time between catching an infectious pathogen and the arrival of its first symptoms. (Note that the incubation period is slightly different to the latency period, the latter being defined as the time between catching a pathogen and the point when the infected person becomes infectious to others – which is the point that the contagious period begins).
The incubation period of this virus can be VERY fast: it can be as fast as 8 hours, but is typically around 12 hours, and generally less than 24 hours. This has been reliably observed: for several infected people, I knew the exact time of exposure to the virus, and the precise time the first symptoms then appeared. I have observed many cases where I know for sure that exposure to this virus happened sometime during a short evening social event (such as an evening dinner), and the subsequent onset of symptoms (vomiting, or sore throat) arrived either in middle of the night, or early next day. All the people that I observed catching this virus in this way later manifested many of the typical long-term sequelae that this virus causes, in the months and years that followed this first infection. Note that irrespective of whether this infection starts with a sore throat, or with a gastrointestinal upset and vomiting (gastroenteritis), in both cases the incubation period is the same: as fast as 8 hours, but typically around 12 hours, and generally less than 24 hours. This unusually rapid incubation period is a good clue to the identity of this virus.
Note: such a rapid incubation period is found in only a few viruses: influenza B viruses have an incubation period of around 24 hours; enterovirus 70 can have an incubation period as fast as 12 hours; rhinoviruses can have an incubation period as fast as 12 hours; norovirus can have an incubation period as fast as 10 hours. So time-wise these viruses could be candidates for the virus described on this website (the virus I caught); but these viruses are not generally known to form persistent long-term infections, as my virus clearly does. Details of incubation periods for some selected viruses are given here.
The prodrome is the nature of the initial symptoms at the beginning of an infection. It has been observed that this viral infection usually starts in one of four ways:-
(1) A sore throat located at the back of the soft palette, on the palatoglossal arch (more towards where this arch meets the tongue on both sides, rather than at the uvula apex of this arch). The infection also develops at the very back of the throat (pharynx), and to a lesser degree in the upper esophagus. The red inflammation (erythema) of this throat infection is clearly discernible on the palatoglossal arch and the pharynx. Inspection of the isthmus faucium area of the pharynx shows both red inflamed skin, and some papules (papules are small raised pimples which are solid rather than fluid-filled and do not produce pus). These papules are slightly elongated rather than round, around 2mm by 1mm in size, and are a slightly whiter shade of red/pink than the surrounding skin. This sore throat looks very similar to a herpangina sore throat, except that in my case, no vesicles (blisters) or ulcers appeared (vesicles and ulcers usually accompany herpangina), only papules. (Note: the name lymphonodular pharyngitis is given to a herpangina-type sore throat where there are only papules; so this may be a better description of the sore throat.) The throat is sore, but with no pain, and very little fever. This throat infection runs for many months before it begins to subside. However it never fully disappears, and usually remains as a chronic sore throat and/or with constant nasal mucus production (although the sore throat becomes a more subdued after a few years). There is an accompanying mild dry cough with little sputum.
(2) Alternatively, the infection can first begin as a gastric upset, with vomiting and diarrhea (in other words, it begins as a viral gastroenteritis or “stomach flu”). In the case of this stomach upset type of prodrome, there is a fever, which lasts for one or two days (unfortunately the fever temperature has not been measured; but it is not unduly high). Significant fatigue is experienced during the fever period. There are no signs of skin rash (at least in the people I observed). The only skin change apparent at this prodrome stage is a slight red flushing, presumed due just to the patient’s temperature.
(3) Sometimes the infection starts with a cluster of lesions and scabs surrounding the facial lips, these lesions looking like large cold sores. In this case, there is also a significant swelling of the lymph nodes in the lower jaw and neck, these swollen lymph nodes easing off after a week or two, as the crusted lesions clear up (these lesions may just be a flare up of pre-existing herpes simplex, as a result of the immunocompromising actions of the chronic sore throat virus; or quite possibly, they may be the oral lesions of hand, foot and mouth disease (HFMD), which is caused by enteroviruses).
(4) Occasionally, this infection can start with just with a viral headache (which can be very intense and can last for two or three days), but no other symptoms (at least initially) other than feeling very irritable, and generally feeling under the weather.
No other prodrome sequences have been noted. NOTE: when the infection begins as a sore throat, a (milder) gastric upset can appear months later. Similarly, when the infection begins as a gastric upset, sore throat can appear weeks later.
Period of Communicability (Contagious Period)
The period of communicability is the time period during which an infected person is infectious to others. The period of communicability is the time period that an infected person is able to transmit their virus to others. For example: in the case of the common cold virus (rhinovirus), this period is the first few days of infection, after which, the body is in recovery from the fever, and the cold virus can no longer be transmitted to others. However, in the case of this chronic sore throat virus, the period of communicability lasts at least a year or so. People with this virus who have a chronic sore throat or constant nasal secretions (which are common symptoms) are able to transmit this virus via the constant source of viral particles shed from the saliva in the mouth and/or from the persistent nasal mucus discharge. I know for sure that I was able to infect someone (via kissing) 15 months after first catching this virus.
The persistent nasal discharge is very characteristic: the constant stuffy nose contains thick, viscous, congested mucus build up. Blowing your nose with a tissue to clear this mucus build-up is necessary every hour or so, and requires a very strong, long blow of the nose to clear out the viscous thick mucus. Once begun, this thick nasal mucus persists indefinitely; it does it start to abate a little after a year or two, but never fully disappears. Exactly the same is true for the sore throat, which persists permanently, but often becoming more subdued in time. NOTE: some people can have the chronic runny nose without the chronic sore throat, and vice versa. Others have both, and other people have neither. Sometimes in infected person will experience a recurrent sore throat, where the throat will clear up for a day or two, but then quickly return. These constant nasopharyngeal symptoms are characteristic, and their persistence means the period of communicability of this virus lasts at least a year or two, perhaps even indefinitely. From my observation, some approximate statistics: about 70% of people with this virus display a chronic stuffy / runny nose, and about 30% get the chronic sore throat.
The contagiousness is how easily an infectious pathogen passes to other people (also called transmission rate). Even though the virus described on this website may have an indefinitely long period of communicability (as a result of its chronic respiratory infection), and even though its incubation period is extremely rapid, by contrast, this virus is not highly contagious. Its person-to-person transmission rate is in fact relatively low. This can be easily deduced from the observation that once one person in a household has caught this virus, it can take over a year before all members of the household have caught it. I have observed this on multiple occasions, in several households.
However, though this virus is only mildly contagious, its communicable period (contagious period) lasts for a long time, at least a year or so (and perhaps even indefinitely). This is why this virus does spread to a lot of people: although it is only weakly contagious, its period of communicability is lengthy, so that there are ample opportunities for it to eventually infect everyone around.
One way this virus can rapidly pass to a person outside the household is when meeting an acquaintance for say lunch or dinner, and having lots of animated conversation while eating on the same table. I have noticed that this tends to pass on the virus. This is almost certainly from oral ejections of tiny globules of spittle that naturally happens during laughing and loud talking. This spittle may land on the table on other person’s food or drink, and then get eaten. Intimate or deep kissing is another way this virus is quite easily transmitted, if the first infected person has the chronic nasopharyngeal infection.
Mental State Changes
About 2 months after the initial prodrome, powerful mental state changes begin (depression, fatigue, apathy, loss of motivation, anhedonia, dysthymia, athymhormia, social withdrawal, a sense of sleepiness, mild dementia, some memory problems, loss of organizational capabilities).
In some people, uncharacteristic outbursts of aggression appear. The severity of the mental state changes varies considerably from person to person: some people are badly affected, others just minimally affected. What is clear is that the mental symptoms, while they do improve a little, linger permanently. Even in those people not particularly badly affected by this virus, episodes of depression, sometimes for days, sometimes protracted over months, seem to be common, even in those sturdy people that had never experienced depression before.
Occasionally, mental state changes can appear straight away on catching this virus, during the first few days of the infection. In this case, though, the mental state changes significantly abate a few days later.
Pins and Needles
About 4 months after the initial prodrome, a “pins and needles” sensation (paresthesias) appears in some people. This tends to be more in the legs, but will often manifest throughout the whole body. Some people with this virus say these pins and needles sensations are located just under the skin; other people say that they are in their muscles. They are transient paresthesias: they come and go.
Receding Gums: Periodontal Disease
Also at 4 months, receding gums and a rapid sudden onset of periodontal disease arises in many people. Dental plaque formation and deposition significantly increases. There may even be new dental caries (tooth decay) suddenly appearing, even for people with excellent oral hygiene habits.
About 12 to 18 months after the initial prodrome, the first signs of fine skin wrinkling are noticed. This closely spaced wrinkling has a texture reminiscent of crêpe paper. These premature skin aging wrinkles start to appear at first on the top of the hands, but the whole body is soon involved. The wrinkled skin produced by this virus looks different in appearance to the look of normal skin aging. For one thing, these virally-precipitated wrinkles are much finer than normal aging wrinkles, with this unusual crêpe paper-like appearance. Also, as we know, normal skin aging happens quite slowly – in normal aging, significant changes in skin appearance are noticeable as the decades go by, not as a year goes by. By contrast, the aging skin process that arises from catching this virus manifests more rapidly, with significant skin changes noticeable within a year or two. The degree of wrinkling this virus causes varies from person to person. Older people (55+) have a greater, and a more rapid increase in body wrinkles, and exhibit slightly deeper wrinkle furrows. Younger people (30 to 55 years) have slightly more shallow furrows. In both cases, however, the wrinkles have this characteristic very fine texture, with crêpe paper-like appearance that are distinct from normal aging wrinkles. People under about 30 or so will tend not to show any of these wrinkles, presumably because their younger skin is more robust in countering the skin-damaging effect of this virus.
Weak Legs and Pelvic Girdle Laxity
Also at 12 to 18 months, the first signs of muscle weakness and looseness appear. The muscle weakness/looseness is primarily located in the the proximal muscles (the muscles in, or closest to, the core of the body). The pelvic girdle muscles (the lower proximal muscles) are most affected; the shoulder muscles are affected to a lesser degree,. Proximal muscle weakness in general is the characteristic of the diseases of dermatomyositis and polymyositis (these two chronic inflammatory myopathy diseases have been linked to coxsackievirus B / enterovirus, and parvovirus B19 infections). Interestingly, lower proximal muscle weakness (hind limb weakness) in particular was found in mice with polymyositis caused by the Tucson strain of coxsackievirus B1 (Refs: 1, 2).
Heliotrope Rash on Chest, and Newly Appearing Dysplastic Nevi Moles
After 2 or 3 years with this virus, further skin symptoms appear. The skin on the upper chest area, just under the neck (the area exposed when wearing a V-neck jumper) develops a little red/pink rash (a heliotrope rash), and the skin texture in this area gets quite thick and oily (or waxy) in texture. Additionally, new moles with a rough texture may appear on the skin; see this picture that I took of one mole that appeared. These type of moles are called atypical moles, or dysplastic nevi.
Author: Hip First Published: May 2007 Last Updated: May 2013