Last update and review: September 22, 2021.
Reactivation of Epstein–Barr virus in COVID-19. Epidemic-level prevalence of active forms of EBV infections and of other herpes virus infections in some geographic area. – blog post.
A short summary.
In this article, we provide a short description of Epstein-Barr virus which is based on a recent review by Stanfield and Luftig, 2017 (2). We also cite and discuss high prevalence of active forms of Epstein-Barr virus observed in COVID-19 patients. The prevalence reported in COVID-19 patients in Moscow area and in critically ill COVID-19 patients in Austira was around 80%. Reactivation of Epstein-Barr virus (EBV) infection by SARS-CoV-2 is a probable explanation. Another explanation is that individuals with active forms of EBV infection have a suppressed immune response and are prone to COVID-19 and severe COVID-19 in particular.
Reactivation of herpes viruses by SARS-CoV-2 infection and vaccination have been reported in literature.
Moscow area has high prevalence of active forms of EBV infections. Active forms of EBV and other herpes viruses were detected in blood donors in Moscow area in Russia. The risk of getting infected with one of the studied herpes viruses for a blood recipient in Moscow was estimated at about 40%.
There is agitation, mass-testing, and self-sabotage in the forms of lockdowns around SARS-CoV-2. However, SARS-CoV-2 variants go extinct in 6 to 12 months. More people are infected with active forms of nasty oncogenic herpes viruses, but no adequate prevention and treatment measures are taken. Thus, schools mass-test only for SARS-CoV-2 and for nothing else.
Our Civilization is in a very low point.
Recent advances in understanding Epstein-Barr virus: several concise notes from the review paper by Stanfield and Luftig, 2017 (2).
Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population.
Stanfield and Luftig, 2017 (2):
“Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population. Infection with EBV is often asymptomatic but can manifest in a range of pathologies from infectious mononucleosis to severe cancers of epithelial and lymphocytic origin. Indeed, in the past decade, EBV has been linked to nearly 10% of all gastric cancers.”
EBV was first identified in 1964 from cultured tumor cells. A reminder: the chimerical Chimp DNA adenovirus from Astra-Zeneca Oxford COVID-19 vaccine is grown in some cancer cells. Do those cancer cells contain some other yet nonidentified viruses? Can those viruses recombine with the chimerical Chimp adenovirus during growth? Who still thinks that we master vaccinology?
Stanfield and Luftig, 2017 (2):
“EBV was first identified in 1964 from cultured tumor cells derived from a patient with Burkitt’s lymphoma (BL).”
Stanfield and Luftig, 2017 (2):
“EBV infection has been associated with a number of different malignancies of both lymphoid and epithelial origin and accounts for 1.8% of all cancer-related deaths worldwide.
EBV is known to encode at least 44 microRNAs (miRNAs). that function in immune evasion by suppressing the release of interleukin-12 (IL-12), disrupting CD4 + T-cell differentiation into type 1 T helper (Th1) cells, and reducing antigen presentation to CD4 + and CD8 + T cells.
Stanfield and Luftig, 2017 (2):
“EBV is known to encode at least 44 microRNAs (miRNAs). Though many of the miRNAs have no known function, it has recently been shown that these virally encoded miRNAs function in immune evasion by specifically suppressing the release of interleukin-12 (IL-12), disrupting CD4 + T-cell differentiation into type 1 T helper (Th1) cells, and reducing antigen presentation to CD4 + and CD8 + T cells. These miRNAs function by interfering with peptide processing, by directly targeting the TAP2 subunit, and by disrupting antigen presentation on MHC-II and MHC-I molecules 14, 15.”
Figure 1 from Stanfield and Luftig, 2017 (2): Initial events of Epstein-Barr virus (EBV) infection.
Stanfield and Luftig, 2017 (2):
“The EBV membrane glycoprotein gp42 binds to its cell surface receptor major histocompatibility complex class II (MHC-II) to initiate entry into the cell. Also, gp350/220 binds to its cell surface receptor CD21 for entry. Interaction with CD21 initiates signaling cascades that prime resting B cells for persistent latent infection. Following endocytosis, the virion and packaged tegument proteins are released into the cytoplasm following fusion of the virion membrane with endosomal membrane. In particular, BNRF1 disrupts the Daxx/ATRX repressor complex to facilitate viral gene expression.”
EBV infection begins in the oral mucosa. Latent infection of epithelial cells can result in nasopharyngeal carcinoma or gastric cancer.
Stanfield and Luftig, 2017 (2):
“Epstein-Barr virus (EBV), also known as human herpes virus 4, is a gamma-herpes. Initial infection with EBV is often asymptomatic but can also manifest as infectious mononucleosis.”
“In vivo, EBV infection begins in the oral mucosa. Replication in epithelial cells is typically lytic; however, latent infection of epithelial cells can result in nasopharyngeal carcinoma or gastric cancer (as discussed in more detail later). After replication in the epithelia, virus is primed for entry into B cells, where a transient growth program is thought to mimic a germinal center reaction, ultimately promoting maturation of the infected cell into the peripheral memory B-cell compartment. Advances in next-generation sequencing and the development of humanized mice have led to better ways to identify and understand the natural strain variation that occurs with EBV. New strain variations, particularly with mutations in latency-associated genes, have been identified in various malignancies. Harnessing these new humanized mice enables studies modeling latent infection and pathogenesis of host-restricted pathogens like HIV and EBV.”
Reactivation of Epstein-Barr virus (Herpesviridae: Lymphocryptovirus, HHV-4) infection during COVID-19 – a study by Solomay et al., 2021 (3).
Subjects: persons of both sexes permanently residing in the territory of Moscow and the Moscow region, aged 18 to 60 years. Hospitalized COVID-19 patients (retrospectively IgG-confirmed) and healthy blood donors.
Solomay et al., 2021 (3):
“In the period from March to May 2020, a cross-sectional randomized study was carried out, which included persons of both sexes permanently residing in the territory of Moscow and the Moscow region, aged 18 to 60 years.
There were 2 groups, comparable to each other by sex and age. The first (patients) included 95 people who were in the hospital for the treatment of a new coronavirus infection, in whom antibodies (AT) of the IgG class to SARS-CoV-2 were retrospectively detected. The second group (blood donors) consisted of 92 participants.”
Detectable prevalence of Epstein-Barr Virus, (inactive and active infection), in Moscow region is 95-100%.
Solomay et al., 2021 (3):
“(Markers of previous) EBV infection (IgG antibodies to EBNA) in the study groups did not have significant differences and amounted to 97.9% (95% CI: 95.0–100.8) in patients and 95.7% (95% CI: 91.5–99.9) among donors.”
10% of blood donors in Moscow have active forms of Epstein-Barr Virus infection.
Reactivation? – In matched hospitalized COVID-19 patients, 80% had markers of active EBV infection.
Solomay et al., 2021 (3):
“Markers of active EBV infection in the donor group were detected in 10.9% of cases (95% CI: 4.5–17.3).For patients, this value was significantly higher both in general (80%; 95% CI: 71.9–88.1) and in each of the subgroups (Table 1).”
Table 1 from Solomay et al., 2021 (3): Frequency of detection of persons with markers of active EBV infection.
Shocking: The cumulative prevalence of active infections by herpes viruses among “healthy” blood donors in Moscow is 27%. The cumulative risk of infection with one of the herpes viruses for a blood recipient is 40.85%.
In another study, the same first author, Salomay, studied the prevalence of several herpes viruses in “healthy” donors admitted to donate blood in Moscow. The prevalence of active infections was shockingly high. These are several on-going epidemics of nasty DNA herpes viruses involved in the pathogenesis of several cancers.
Adapted from Solomay et al., 2021 (4):
“Active forms (of infection) with EBV was 11.97%. Frequency of blood donors with active infections caused by herpes simplex, types 1 and 2, EBV, cytomegalovirus, and human herpes type 6 virus amounted to 27.46/100 examined. Risk of infection with examined herpes viruses during blood transfusions were to 40.85/100 recipients.”
Compare the 11.97% prevalence of active forms of EBV in Moscow area with the prevalence of SARS-CoV-2. In a “64%-fully vaccinated Israel”, in the beginning of September 2021, there were 117 new daily cases per 100 thousand of population. 117 new daily cases is very high, among the highest levels seen in different countries during the one and a half years of COVID-19 epidemic.
117 new daily cases amounts to 0.117% of the population being infected each day. Prevalence is the proportion of people in a population that have a disease or are asymptomatic carriers of a pathogen at the same time. We can assume that viral RNA is detectable during 10 days on average. After 10 days, infectious SARS-CoV-2 virus is detectable in a minority of the infected. We can, thus, calculate the prevalence of SARS-CoV-2 infection as 0.117%(infected each day)*10(the average presence of infectious virus in days)=1.17% during the worst epidemic peak.
Figure: Epidemilogic situation in a “64%-fully vaccinated” Israel as of September 4, 2021.
But if we examine different SARS-CoV-2 variants, we can see that the prevalence of many of the variants is currently zero or close to zero. Indeed, the original Wuhan variant, and several other variants are alomst extinct. Thus, in France, by August 3, 2021, 98% of detected infectious viruses were the Delta (or Indian) variant. All other variants, therefore, were only 2%.
The New Neander’s Medical on September 20, 2021:
Official French Medical Statistics: “Variants: Delta variant (was) identified in 98.1% of cases by sequencing in mainland France on August 3, 2021.” Analysis: Healthcare professionals are being forced to get vaccinated against SARS-CoV-2 variants that have already disappeared.”
Why schools don’t test for active infections with herpes viruses, including Epstein-Barr Virus?
Given the high prevalence of active forms of infections with herpes viruses, schools and other institutions should be testing also for those infections. And for many others. Why it is not done? Why bureaucrats are so agitated only about SARS-CoV-2?
Reactivation of herpes simplex keratitis following vaccination for COVID-19 – a report by Richardson-May et al., 2021 (5).
Richardson-May et al., 2021 (5):
“An 82-year-old man with a history of herpes simplex keratitis 40 years previously presented with recurrence, 1 day following vaccination for novel COVID-19. His condition worsened despite topical treatment with ganciclovir gel. A diagnosis of herpetic stromal keratitis was made, requiring systemic aciclovir, topical prednisolone, moxifloxacin and atropine, and oral doxycycline. He improved clinically on treatment, with some residual corneal scarring. Visual acuity improved from 6/36 corrected at presentation, to 6/24 following treatment.”
HSV-1 and HSV-2 are common, double-stranded, non-enveloped DNA viruses. 52%–84% of adults demonstrate latent infection to HSV-1.
Richardson-May et al., 2021 (5):
“HSV-1 and HSV-2 are common, double-stranded, non-enveloped DNA viruses. Ocular infection can cause a range of conditions. In the cornea, this includes epithelial, stromal and disciform keratitis. Other ocular conditions include blepharoconjunctivitis, iridocyclitis and retinal infection such as acute retinal necrosis.1 Approximately 52%–84% of adults demonstrate latent infection to HSV-1.2 Latent infection within the trigeminal ganglia, along with recurrent episodes of viral replication, can lead to recurrent clinical disease; this can include corneal infection, as in our patient.”
Walter et al described reactivation of herpes virus infection in mostly healthy subjects with no relevant comorbidity following vaccination.
Figure 1 from Richardson-May et al., 2021 (5): The patient’s clinical appearance 1 week after beginning topical treatment.
Richardson-May et al., 2021 (5):
“The eye is significantly inflamed, with corneal neovascularisation, epithelial defect and stromal opacity. The pupil is pharmacologically dilated.”
Hassman and DiLoreto described a patient with previous HSV-1 encephalitis, who later developed acute retinal necrosis 1 day following an influenza vaccine.
Richardson-May et al., 2021 (5):
“Hassman and DiLoreto described a patient with previous HSV-1 encephalitis, who later developed acute retinal necrosis 1 day following an influenza vaccine. PCR of the aqueous fluid was positive for HSV-1.3 Reactivation of cutaneous HSV-2 has been reported in a patient with transverse myelitis following influenza vaccination.4 Grillo and Fraunfelder, identified 24 causes of keratitis following vaccination for varicella zoster; most of these occurred within days, and resolved with topical steroid and oral aciclovir. They suggested that persistent viral antigens within the cornea may be the underlying mechanism.5 Walter et al described reactivation of herpes virus infection in mostly healthy subjects with no relevant comorbidity following vaccination.6”
Possible mechanisms for reactivation of HSV following vaccination include … autoinflammation triggered by the vaccine, with possible reduction in neurotrophin allowing HSV replication; this has been demonstrated within the brain following intranasal H1N1 influenza vaccination.
Richardson-May et al., 2021 (5):
“Possible mechanisms for reactivation of HSV following vaccination include … autoinflammation triggered by the vaccine, with possible reduction in neurotrophin allowing HSV replication; this has been demonstrated within the brain following intranasal H1N1 influenza vaccination.3 7 Further, distraction of humoral response due to the vaccination may lead to loss of immunological control of HSV.3
To our knowledge, this is the first reported case of reactivation of herpes simplex keratitis following vaccination for COVID-19, with a clear temporal relationship.”
The study by Lehner et al., 2020 (1): “78% of invasively ventilated COVID-19 patients had Epstein-Barr Virus viremia.”
The data on high prevalence of active Epstein-Barr Virus infections in COVID-19 patients are confirmed by a small study in Austrian intensive care units.
Invasively ventilated COVID-19 patients showed biochemical abnormalities that resemble hepatitis and pancreatitis typically caused by herpesviruses like Epstein–Barr virus (EBV) or cytomegalia virus (CMV).
Lehner et al., 2020 (1):
“We observed that COVID-19 patients invasively ventilated in our intensive care unit (ICU) showed biochemical abnormalities that resemble hepatitis and pancreatitis typically caused by herpesviruses like Epstein–Barr virus (EBV) or cytomegalia virus (CMV). Moreover, a subgroup of COVID-19 patients exhibit a hyperinflammatory pattern similar to secondary hemophagocytic lymphohistiocytosis (sHLH) [1, 2], a syndrome that can be triggered by viruses like EBV. Tus, we speculated whether critically ill COVID-19 patients show evidence of EBV- or CMV-infection or reactivation and quantifed EBV as well as CMV DNA levels in blood by PCR.”
78% of invasively ventilated COVID-19 patients had EBV viremia, 39% even above 1000 IU/ml. Prevalence and levels of EBV viremia were signifcantly higher in COVID-19 patients compared to non-COVID-19 patients (44.4%).
“We found that 78% of COVID-19 patients had EBV viremia, 39% even above 1000 IU/ml. Prevalence and levels of EBV viremia were signifcantly higher in COVID-19 patients compared to non-COVID-19 patients (44.4%, Pearson Chi-square p = 0.040, Mann–Whitney Utest p = 0.022, SPSS 26 (IBM, Armonk, NY)). In contrast, only 17% of COVID-19 patients and 5.6% of non-COVID-19 patients had evidence of CMV viremia, which was not signifcantly diferent between the groups (Pearson Chi-square p = 0.289).”
In Austria, patients with relatively low CRP levels are put on invasive mechanical ventilation. This is a possible case of malpractice.
The following “table 1” from the study by Lehner et al., 2020 (1), contains a piece of rather troubling information. Indeed, the C-reactive protein level in patients on mechanical ventilation appears low (median (interquartile range): 15.5 (7.7-19.7)mg/dL. It is possible that these patients are receiving corticosteroids and their CRP levels are, thus, suppressed by this treatment. However, this still looks like a case of malpractice. Indeed, the table does not contain any information that would indicated that intubation was justified.
There was a signifcant correlation between EBV viremia and interleukin-6 (IL-6) level (Fig. 1, r = 0.621, p = 0.006) in COVID-19 patients, but not in non-COVID-19 patients.
Lehner et al., 2020 (1):
“No correlations between viral load of EBV and blood levels of hepatic and pancreatic enzymes or cholestasis parameters were detected. However, there was a signifcant correlation between EBV viremia and interleukin-6 (IL-6) level (Fig. 1, r = 0.621, p = 0.006) in COVID-19 patients, but not in non-COVID-19 patients (r = − 0.195, p = 0.438, Spearman’s rank-order correlation.”
“Since EBV can induce immune dysregulation and expression of IL-6 in peripheral blood mononuclear cells (PBMCs) in vitro [3], one might speculate that EBV acts as an additional infammatory trigger in critically ill COVID-19 patients.”
Lehner et al., 2020 (1):
“This is the frst systematic report of EBV viremia in critically ill COVID-19 patients which revealed two important fndings: First, COVID-19 patients have a higher prevalence of EBV viremia compared to non-COVID-19 patients. Second, levels of EBV viremia correlate with IL-6 in COVID-19 patients but not in non-COVID-19 patients. Since EBV can induce immune dysregulation and expression of IL-6 in peripheral blood mononuclear cells (PBMCs) via deoxyuridine triphosphate nucleotidohydrolase (dUTPase) in vitro [3], one might speculate that EBV acts as an additional infammatory trigger in critically ill COVID-19 patients. Te observation that two patients without history of allergy but an EBV viremia above 1000 IU/ml developed a generalized maculopapular rash following administration of amoxicillin/clavulanate and piperacillin/tazobactam, further emphasizes the hypothesized immunological impact of EBV in this setting [4, 5]. Although this observation was made in a limited number of patients in a retrospective analysis, the systematic approach based on registry data minimizes the risk of selection bias. Moreover, we compared COVID-19 patients to an appropriate control group. Te fndings concerning EBV and CMV viremia in the control group are in accordance with previously reported cumulative incidences (i.e., 48% and 18%, respectively) [6].”
Conclusions by Lehner et al., 2020 (1): EBV viremia is highly prevalent in COVID-19 patients with respiratory failure.
Lehner et al., 2020 (1):
“These data suggest that EBV viremia is highly prevalent in COVID-19 patients with respiratory failure and associated with systemic infammation as evidenced by high IL-6 levels. It remains to be elucidated whether EBV.”
Conclusions.
Around SARS-CoV-2, there is agitation, mass-testing, forced-vaccination with dangerous and ineffective vaccines, as well as self-sabotage in the form of lockdowns. However, SARS-CoV-2 variants go extinct in 6 to 12 months. More people are infected with nasty oncogenic herpes viruses, but no adequate prevention measures are taken. Thus, schools mass-test only for SARS-CoV-2 and for nothing else.
Our Civilization is in a very low point.
Selected references:
1. Lehner et al. Crit Care (2020) 24:657.
2. Stanfield and Luftig. F1000Research 2017, 6(F1000 Faculty Rev):386
3. Solomay TV, Semenenko TA, Filatov NN, Vedunova SL, Lavrov VF, Smirnova DI, Gracheva AV, Faizuloev EB. [Reactivation of Epstein-Barr virus (Herpesviridae: Lymphocryptovirus, HHV-4) infection during COVID-19: epidemiological features]. Vopr Virusol. 2021 May 15;66(2):152-161. Russian. doi: 10.36233/0507-4088-40. PMID: 33993685.
4. Solomay T.V., Semenenko T.A., Karazhas N.V., Rybalkina T.N., Kornienko M.N., Bosh’yan R.E., Golosova S.A., Ivanova I.V. Assessing risks of infection with herpes viruses during transfusion of donor blood and its components. Health Risk Analysis, 2020, no. 2, pp. 135–142. DOI: 10.21668/health.risk/2020.2.15.eng
5. Richardson-May J, Rothwell A, Rashid M Reactivation of herpes simplex keratitis following vaccination for COVID-19 BMJ Case Reports CP 2021;14:e245792.