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Abortive infection theory of ME/CFS
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== Dr A Martin Lerner's Abortive Infection Theory of ME/CFS == Dr Lerner explains his abortive infection theory of ME/CFS in his 2011 paper: <blockquote>We propose that ME/CFS patients have nonpermissive herpesvirus (EBV, HCMV, HHV6) replication, expressing immediate-early (IE) gene products, which induce host cell dysregulation and host cell apoptosis<ref>{{Cite journal|title=A paradigm linking herpesvirus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome|date=2011-02|url=http://www.dovepress.com/a-paradigm-linking-herpesvirus-immediate-early-gene-expression-apoptos-peer-reviewed-article-VAAT|journal=Virus Adaptation and Treatment|pages=19|last=Lerner|first=Martin|last2=Lerner|language=en|doi=10.2147/VAAT.S15105|issn=1179-1624}}</ref></blockquote>By "non-permissive herpesvirus replication," Dr Lerner means an abortive herpesvirus infection in non-permissive cells. Note that Dr Lerner often refers to abortive infections as "non-permissive infections", although strictly speaking, the term non-permissive refers to cells, not to infections (cells in which abortive infections can arise). Dr Lerner says in the same paper that:<blockquote>EBV ME/CFS subset patients also have uniquely elevated serum antibody titers to the nonstructural gene products EBV-specific DNase and DNA polymerase. These elevated EBV-specific serum antibody titers are also present in patients with EBV-related malignancies, Burkittβs lymphoma, and nasopharyngeal carcinoma, but are not present in patients with infectious mononucleosis or in healthy individuals.</blockquote>So ME/CFS patients are producing antibodies to nonstructural proteins made by viruses. This might be because in abortive infections, there may be higher levels of nonstructural proteins, and a lack of structural viral capsid proteins (since in abortive infections, full virions are not constructed). Dr Lerner says that the diffuse and restricted component of Epstein-Barr virus (EBV) early antigen (EA) indicates abortive EBV viral infection.<ref>{{Cite web|url=http://web.archive.org/web/20140104024937/http://www.treatmentcenterforcfs.com/links/documents/AMLEBVReviewPressRelease9.23.10.pdf|title=Causal Relationship Identified Between Epstein Barr Virus and Chronic Fatigue Syndrome. Press release September 23, 2010.|last=Lerner|first=A Martin}}</ref> In his 2012 paper, Dr Lerner finds that in 106 ME/CFS patients with herpesvirus infections, 81% had elevated early antibodies, to EBV early antigen (diffuse). Dr Lerner also found antibodies to deoxyuridine triphosphatase (dUTPase) from EBV and EBV DNA polymerase.<ref>{{Cite journal|title=Abortive lytic Epstein–Barr virus replication in tonsil-B lymphocytes in infectious mononucleosis and a subset of the chronic fatigue syndrome|date=2012-11|url=http://www.dovepress.com/abortive-lytic-epsteinndashbarr-virus-replication-in-tonsil-b-lymphocy-peer-reviewed-article-VAAT|journal=Virus Adaptation and Treatment|pages=85|last=Lerner|first=Martin|last2=Beqaj|first2=Safedin|language=en|doi=10.2147/VAAT.S36540|issn=1179-1624}}</ref> dUTPase is a viral enzyme produced in both productive and abortive infections. EBV-encoded dUTPase has been shown to induce sickness behavior symptoms (which are similar to ME/CFS symptoms).<ref>{{Cite journal|title=Epstein-Barr virus-encoded dUTPase modulates immune function and induces sickness behavior in mice|date=2004-11|url=https://pubmed.ncbi.nlm.nih.gov/15368518/|journal=Journal of Medical Virology|volume=74|issue=3|pages=442β448|last=Padgett|first=David A.|last2=Hotchkiss|first2=Andrew K.|last3=Pyter|first3=Leah M.|last4=Nelson|first4=Randy J.|last5=Yang|first5=Eric|last6=Yeh|first6=Peir-En|last7=Litsky|first7=Monica|last8=Williams|first8=Marshall|last9=Glaser|first9=Ronald|doi=10.1002/jmv.20196|pmid=15368518|issn=0146-6615}}</ref> In his 2008 paper on cytomegalovirus in ME/CFS,<ref>{{Cite journal|title=Immunoassay with cytomegalovirus early antigens from gene products p52 and CM2 (UL44 and UL57) detects active infection in patients with chronic fatigue syndrome|date=2008-05|url=https://pubmed.ncbi.nlm.nih.gov/18037660/|journal=Journal of Clinical Pathology|volume=61|issue=5|pages=623β626|last=Beqaj|first=S. H.|last2=Lerner|first2=A. M.|last3=Fitzgerald|first3=J. T.|doi=10.1136/jcp.2007.050633|pmid=18037660|issn=1472-4146}}</ref> Dr Lerner says that:<blockquote>The p52, CM2 recombinant IgM assay to early human cytomegalovirus (HCMV) antigens is diagnostic of abortive HCMV infection.</blockquote><blockquote>These results confirm our previous findings that p52 and CM2 serum antibodies are specific in diagnosis of HCMV abortive infection in CFS patients similar to those infected with EBV. In that study, p52 and CM2 HCMV IgM serum antibody titres were present in this HCMV subset of CFS patients, but not in control non-CFS patients. In turn, the presence of p52 and CM2 antibodies to p52 and CM2 non-structural antigens may account for difficulties in detecting HCMV DNA in blood or cardiac biopsies in these CFS patients, consistent with the paradigm of incomplete or abortive viral multiplication. Abortive viral multiplication in immunocompetent CFS patients may be unique</blockquote>A team at Ohio State University have also discovered that antibodies to herpesvirus dUTPase are more common in ME/CFS patients: they found 31% to 53% of ME/CFS patients have high levels of antibodies to the dUTPase protein produced by EBV, HHV-6 and VZV.<ref>{{Cite journal|title=Myalgic encephalomyelitis/chronic fatigue syndrome and gulf war illness patients exhibit increased humoral responses to the herpesviruses-encoded dUTPase: Implications in disease pathophysiology|date=2017-09|url=https://pubmed.ncbi.nlm.nih.gov/28303641/|journal=Journal of Medical Virology|volume=89|issue=9|pages=1636β1645|last=Halpin|first=Peter|last2=Williams|first2=Marshall Vance|last3=Klimas|first3=Nancy G.|last4=Fletcher|first4=Mary Ann|last5=Barnes|first5=Zachary|last6=Ariza|first6=Maria Eugenia|doi=10.1002/jmv.24810|pmc=5513753|pmid=28303641|issn=1096-9071}}</ref><ref>{{Citation|title=The Role of EBV-dUTPase in Modulating Neuro-Immune Dysfunction Associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome|date=2020-05|url=https://kb.osu.edu/handle/1811/91637|last=Hasik|first=Julia|access-date=2023-08-30|language=en-US}}</ref> Ohio State believe dUTPase may be a biomarker in a subset of ME/CFS patients.
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