Coxsackievirus B4 sewage-isolate induces pancreatitis after oral infection of mice

Abstract

Numerous serotypes which belong to the genus Enterovirus (EV) show variability in their virulence and clinical manifestations. They are also known to undergo changes caused by mutations and recombination during their circulation in the environment and the population. Various EV serotypes are prevalent in groundwater, wastewater, and surface waters. Our previous studies showed that oral infection induces pancreatitis depending on specific conditions, such as gravidity, in an outbred murine model. Our aim in the present study was to further explore the pancreatic histopathology in an outbred mouse model following oral infection with clinical isolates from a patient who had aseptic meningitis and an isolate from a treated-sewage sample recovered from the residential area of the patient. The isolates were identified as coxsackievirus B4 (CVB4) in tissue culture. The CVB4 sewage-isolate induced pancreatitis after oral infection. In contrast, pancreatitis was absent following infection with the clinical isolates. Comparison of polyprotein sequences showed that the treated-sewage strains differed from the patient's isolates by 9 and 11 amino acids. We conclude that the isolates of clinical and environmental origin differed in their pathogenic properties and showed genetic variation.

Severe pneumonia and pathogenic damage in human airway epithelium caused by Coxsackievirus B4

“…Throat swab samples from 3 CVB4-positive patients (Ct values ranged from 25 to 29) were used for viral culture. However, permissive cells commonly used to culture CVB4 from stool or cerebrospinal fluid, such as LLC-MK2 or RD cells [ 37 ], were not successfully cultivated. Therefore, in this study, eight other kinds of cell lines were used to select cells susceptible to pneumonia-derived CVB4 inoculation.…”

Screening of a new candidate coxsackievirus B1 vaccine strain based on its biological characteristics

“…To sum it up, these findings provided further support for the association between CVB1 infection and meningitis, myocarditis, hepatitis, pancreatitis, and T1DM. In addition, previous research also found that different CVB4 isolates could induce different diseases (Benkoova et al, 2021), and CVB has a high frequency of mutations that may result in changes in pathogenicity (Beck et al, 1995); the high mutation frequency of the CVB1 strain might lead to hepatitis (Wang et al, 1998). In addition, the KM7-X29 P10 strain was as pathogenic as its original strain, KM7, in mice (data not shown).…”