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Certain strains of coxsackievirus A-9 induce minimal necrosis and interstitial inflammation of the murine heart (1, 2). Although affected mice appear well, cardiac size is increased. During the first 2 wk of infection, virus is present in the heart. When examined later, these myocardia are normal in size and are free of histologic change (3-5). Swimming increases myocardial replication of virus but does not alter the benignity of the process (6).On the other hand, when weanling mice are inoctflated with coxsackievirus B-3 (Nancy), a necrotic carditis involving 25-50% of the entire myocardiUm results. As with coxsackievirus A-9, coxsackievirus B-3 may be isolated only very early. Here, too, the infected baby mice continue to appear well. However, in the case of coxsackievirus B-3, healing is accompanied by myocardial fibrosis, deposition of calcium, and continuing inflammation. Since the continuing carditis is not associated with virus multiplication, we have called the entire process a myocardiopathy (7-9).Human cardiac disease occurs, similar to that caused by the benign coxsackievirus A-9 and having lesions similar to the murine lesions caused by the virulent coxsackievirus B-3. The present experiments bring striking data to bear upon the role of the exercise induced by swimming upon routine coxsackievirus B-3 myocardiopathy. Materials and MethodsMice.--Pregnant albino Swiss ICR mice were obtained at term. After delivery, each mother with its brood was housed in a separate cage. Nurslings were weaned at about 3 wk and, thereafter, were fed standard Rockland rat chow.

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BackgroundA defined diagnostic panel differentiated patients who had been diagnosed with chronic fatigue syndrome (CFS), based upon Fukuda/Carruthers criteria. This diagnostic panel identified an Epstein-Barr virus (EBV) subset of patients (6), excluding for the first time other similar “clinical” conditions such as cytomegalovirus (CMV), human herpesvirus 6 (HHV6), babesiosis, ehrlichiosis, borreliosis, Mycoplasma pneumoniae, Chlamydia pneumoniae, and adult rheumatic fever, which may be mistakenly called CFS. CFS patients were treated with valacyclovir (14.3 mg/kg q6h) for ≥12 months. Each patient improved, based upon the Functional Activity Appraisal: Energy Index Score Healthcare Worker Assessment (EIPS), which is a validated (FSS-9), item scale with high degree of internal consistency measured by Cronbach's alpha.MethodsAntibody to EBV viral capsid antigen (VCA) IgM, EBV Diffuse Early Antigen EA(D), and neutralizing antibodies against EBV-encoded DNA polymerase and EBV-encoded dUTPase were assayed serially approximately every three months for 13–16 months from sera obtained from patients with CFS (6) and from sera obtained from twenty patients who had no history of CFS.ResultsAntibodies to EBV EA(D) and neutralizing antibodies against the encoded-proteins EBV DNA polymerase and deoxyuridine triphosphate nucleotidohydrolase (dUTPase) were present in the EBV subset CFS patients. Of the sera samples obtained from patients with CFS 93.9% were positive for EA(D), while 31.6% of the control patients were positive for EBV EA(D). Serum samples were positive for neutralizing antibodies against the EBV-encoded dUTPase (23/52; 44.2%) and DNA polymerase (41/52; 78.8%) in EBV subset CFS patients, but negative in sera of controls.ConclusionsThere is prolonged elevated antibody level against the encoded proteins EBV dUTPase and EBV DNA polymerase in a subset of CFS patients, suggesting that this antibody panel could be used to identify these patients, if these preliminary findings are corroborated by studies with a larger number of EBV subset CFS patients.

In this study, we found that neutralizing antibody responses in COVID-19-convalescent individuals vary in magnitude but are durable and correlate well with receptor binding domain (RBD) Ig binding antibody levels compared to other SARS-CoV-2 antigen responses. In our cohort, higher neutralizing antibody titers are independently and significantly associated with male sex compared to female sex.

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Coxsackieviruses B1-B4 were inoculated intraperitoneally into 48-hr-old, 14-day-old, and three- to five-month-old Swiss-Webster mice. Immediate death occurred only among mice less than 48 hr old, which died from fulminant encephalitis. Older mice usually survived. Myocarditis ensued in mice less than 48 hr old that were infected with coxsackieviruses B1 and B4. Several of the surviving mice developed left ventricular aneurysms, which resulted from transmural necrotizing myocarditis. In this group (coxsackieviruses B1 and B4), pathologic changes in the heart were synchronous with maximal cardiac titers of virus. Fourteen-day-old mice infected with coxsackieviruses B2 and B3 developed nontransmural necrotizing myocarditis in which maximal pathologic changes followed peak cardiac titers of virus by several days, whereas three- to five-month-old mice infected with coxsackieviruses B1, B2, B3, or B4 showed maximal susceptibility to destructive lesions in the exocrine glandular pancreas. Therefore, specific susceptibilities to infection with coxsackieviruses group B vary with age of the mouse, virus type (and strain), and organ.