It is important that the original content is preserved. This is provided as an update.

Long Covid may be triggered by dormant viruses behind cold sores and chickenpox as scientists investigate link

 

https://inews.co.uk/news/science/long-covid-viruses-infections-cold-sores-chickenpox-1132349

As proposed 1 year ago, long Covid and the unusual and extreme symtons may be due to a dormant virus. EBV virus or Epstein Barr Virus is being considered alongside HSV. Out of the two only HSV is known to be able to breach the blood brain barrier. Reference to https://inews.co.uk/news/science/long-covid-viruses-infections-cold-sores-chickenpox-1132349

"These same findings were also seen by Massimo Galli, Professor of Infectious Diseases at the University of Milan, though he has been too busy to  quantify the finding. He also noted that these peculiar symptoms were also noted later in the course of infection so won’t be of value as a clue to early diagnosis.
Having practiced infectious disease for forty years now, the only other infection I’ve seen with a loss of smell was Herpes simplex encephalitis, so I was intrigued by this unusual symptom." Ref : Judy Stone, Forbes Mar 20, 2020 Apple News - https://www.forbes.com/sites/judystone/2020/03/20/theres-an-unexpected-loss-of-smell-and-taste-in-coronavirus-patients/#69c0fdbc5101

So the most dangerous symptoms of Covid 19 are likely to be linked to a breach of the Blood Brain Barrier and the key to treating and preventing Covid 19 and Long Covid are in treating HSV.

There is a very effective treatment for HSV. Discovered over 30 years ago and this treatment has been surpressed by parties who will not entertain the idea that Chronic Fatigue Syndrone is an actual thing and not merely, accoring to Professor Simon Wessely "Like it or not, CFS is not simply an illness, but a cultural phenomenon and metaphor for our times.".

There are treatments that are being trialled for HSV, One of the most notable being William Pridgen M.D. of Innovative Med Concepts.

There is also a treatment that was discovered more than 30 years ago. This treatment showed promise in clinical trials to find a treatment for Schizophrenia.

I am choosing to not post the treatment here since it must be put in context. Of a life's search for a cure for HSV and a belief in it's role in Alzheimer's, Diabetes and Neurological issues due to heading a ball.

This is not an attempt to gain a patent on the treatment but more an attempt to give everyone the access to the treatment regardless of country or idealogical barriers.

 

 

 

 

 

It is very likely that the coronavirus will depend on the Herpes simplex viruses to infect and cause serious illness in humans. Almost all the bodies’ defences against viruses, can be disabled by the HSV’s. In various ethnic groups, there is wide variation in pathogen burden, which corresponds with the mortality from coronavirus infections. Treatment with anti-HSV drugs, could be of benefit to those infected with coronavirus, although prophylactic treatment could be of the greatest benefit.

An estimated 3.7 billion people under age 50 (67%) have HSV-1 infection globally.
Both oral herpes infections and genital herpes infections are mostly asymptomatic or unrecognized but can cause symptoms of painful blisters or ulcers at the site of infection, ranging from mild to severe.

The herpes simplex virus is categorized into 2 types: herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2).

HSV-1 is mainly transmitted by oral-to-oral contact to cause oral herpes (which can include symptoms known as “cold sores”), but can also cause genital herpes.

A characteristic of the human herpes viruses is their ability to remain latent in the neurons for life.
They can then reactivate under a number of circumstances. These triggers include: heat and cold, stress, trauma and of relevance in the present context, infection by other viruses.

Infection with HSV-2 increases the risk of acquiring and transmitting HIV infection.

Whether or not COV is able to reactivate HSV, there could be a number of consequences of especial importance, in the ability of both HSV-1 and HSV-2 to disable many of the bodies’ defences against viruses (Tognarelli, Palomino, Corrales et al. 2019). In their review paper they discuss the evidence for the ability of both HSV-1 and HSV-2 to evade host early innate antiviral responses. If HSV-infected cells are unable to restrict the replication of HSV’s, an innate immune response, consisting of both acellular and various cell types can interact with the virus or infected cells, to try to avoid infection of adjacent cells or other tissues. Additionally, glycoprotein C on the surface of the virus, can bind to the complement component C3b and block the formation of a membrane attack complex on the surface of the virus and infected cells. Natural killer (NK) cells are innate immune cells that are capable of recognising and destroying virus infected cells, which either lack the expression of major histocompatibility complex molecules or express NK-activating molecules on the surface, because abnormal cellular processes betray infection.
Other viral products can downregulate NK surface ligands, leading to protection of virus infected cells from NK mediated apoptosis.
HSV, via its glycoprotein B, can inactivate the natural killer cells (Rao P et al. 2011) which are the first line of defence against viruses and tumour cells.

Another ability of HSV, is to damage the blood brain barrier (BBB), allowing other viruses, bacteria and micro-organisms to enter the brain. Relatively few viruses can cause such damage to the BBB. These include, besides HSV, HIV (Mc Rae, 2016. Spindler KR, Hsu TH, 2012) and a few less well known viruses, such as West Bile fever Rift Valley Fever, Japanese encephalitis. Chikungunya, human t cell leukemia 1 and rabies virus (Hou J, Baker LA, Zhou L, Klein RS. 2016).

These attacks, by HSV’s on the body’s defence against viruses, could facilitate infection by COV, which, in the absence of HSV’s, could be difficult or even impossible.

HSV’s 1 and 2 could well determine the severity of COV infections by allowing COV to enter the body unopposed, multiply and reach the central nervous system.

The COVID-19 pandemic has dominated the thoughts of people around the world. It appears to be totally indiscriminate. However, when you see the pictures of NHS workers who have died from coronavirus (COV), it is obvious that mortality amongst ethnic minorities is disproportionately high. While looking through the scientific literature for an explanation, I came across a paper that gave an insight into a possible cause. It was entitled: “Persistent socioeconomic and racial and ethnic disparities in pathogen burden in the United States, 1999-2014 (R. C. Stebbins, G E Noppert, A E Aiello et al. Epidemiol Infect. 2019; 147: e 301.) They examined data from 17,660 participants in the National Health and Nutrition Survey participants. They looked at “Pathogen Burden”, which was arrived at by the number of positive serologies for cytomegalovirus (CNV), herpes simplex virus-1(HSV) and HSV-2, human papilloma virus and the parasite: Toxoplasma gondii and dividing by the number of parasites tested, giving a percent-seropositive for each participant. They examined sex- and age- adjusted mean pathogen burdens from 1999-2014, stratified by race, ethnicity, poverty to income ratio (PIR) and educational attainment. Those with a PIR < 1.3, had mean pathogen burden (MPB) 1.4-1.8 times those with a PIR > 3.5, with no change over time. Disparities in education had even greater effect, with the MPB among those that had less than a high school education being around twice that of those who had completed more than a high school education. Non-Hispanic black, Mexican American and other Hispanic participants had a mean pathogen 1.3-1.9 times that of non-Hispanic Whites. They demonstrated that the socio-economic and racial/ethnic disparities in pathogen burden have persisted over 16 years, with no sign that the gap is closing. My suspicion is that living in extended families, more crowded housing and probably several other factors, could account for these disparities Having seen that these disparities do exist I will suggest a reason why mortality from COV should be different amongst among racial and ethnic groups and also among the socially deprived. The most frequent pathogen in the study was HSV-1. This virus, although being largely associated with cold sores, genital lesions and encephalitis has other capabilities which are less obvious. Both HSV-1 and HSV-2 can go into latency and cause life-long infections in the neurons of the host. Especially pertinent in the present context, is their effects on the immune system. A paper entitled “Herpes simplex virus evasion of early host antiviral responses” (E I Tognarelli, T F Tognarelli, N Comares et al. Front Cell Infect Microbiol. 2019; 9: 127.). reviews most of the actions by which HSV-1 and HSV-2 can avoid or inactivate most of the host’s antiviral responses. Natural killer cells (NK) are one of the first lines of defence against viruses and tumour cells. They can recognise and destroy virus infected cells that either lack the expression of major histocompatibility complex-1 molecules or express NK- activating on the cell surface because of abnormal cell processes betray infection. There are many other processes by which HSV can evade the body’s ability to counteract virus invasions. All these will enable COV to invade and reach almost all parts of the body unopposed. Many other means by which HSV can damage other immune cells and processes are discussed in this paper but all of these underline why increased pathogen burden could result in greater mortality in groups with higher “pathogen burdens.

1. Desai DV, Kulkami SS. Herpes simplex virus: the interplay between HSV, host, and HIV-1. Viral Immunol. 2015; 28:546-555.
2. Schiffer JT, Gottlieb SL Biologic interactions between HSV-2 and HIV-1 and possible implications for HSV vaccine development. Vaccine; 2019; 37:7363-7371.
3. Bond PA. A role for herpes simplex in the aetiology of chronic fatigue syndrome and related disorders. Medical Hypotheses, 1993; 40: 301-308.
4. Pridgen WL, Duffy C, Gendreau JF, Gendreau RM. A famciclovir + celecoxib combination treatment is safe and efficacious in the treatment of fibromyalgia. J Pain Res. 2017; 10: 451-
5. Rao P, Pham HT, Kulkami A, Yang Y et al. Herpes simplex virus 1 glycoprotein B and US3 collaborate to inhibit CD1d antigen presentation and NKT cell function. J Virol. 2011; 85: 8093-8104.
6. McRae M. HIV and viral protein effects on the blood brain barrier. Tissue barriers. 2016; 4: 1142543.
7. Spindier KR, Hsu TH. Viral disruption of the blood-brain barrier. Trends microbiol. 2012; 20: 282-290.
8. Hou J, Baker LA, Zhou L, Klein RS. Viral interactions with the blood-brain barrier: old dog, new tricks. Tissue barriers. 2016; 4: e1142492.
9. Tognarelli I, Palomino TF, Corrales F, Bueno SM, et al. Herpes simplex virus evasion of early host antiviral responses. Front Cell Microbiol. 2019; 9: 127.
10. Stebbins RC, Noppert GA, Allelo AE, Cordoba E, Ward JB, Feinstein L. Persistent socioeconomic and ethnic disparities in pathogen burden in the United States, 1999-2014. Epidemiol Infect. 2019; 147: e301.