Coxsackievirus B3 infection alters plasma membrane of neonatal skin fibroblasts

Abstract

Replication of coxsackievirus B3 occurred for days in cultures of murine neonatal skin fibroblasts in the absence of cytopathology and resulted in alteration of the plasma membrane. Dual immunofluorescence studies showed that the lectin Ulex europaeus agglutinin I bound only to cells producing viral capsid antigens. Cultures of coxsackievirus B3-inoculated murine neonatal skin fibroblasts showed maximum binding of this lectin at 72 h postinoculation. These data show that in a nonlytic infection a picornavirus can alter the surface of an infected cell.

Serological probes for some foot-and-mouth disease virus nonstructural proteins

“…This is observable only transiently about 2 hours post-infection. Similarly located aggregates have been described for cells infected by the Theiler virus in vivo (18), and infection-dependent alteration of the cell surface has been found with Coxsackie B3 virus (19); however, each time it was without specification of the responsible protein. Poliovirus-infected cells, on the other hand, accumulate the 2C analogue in vesicles built by the endoplasmatic reticulum (20).…”

Attenuation of a reactivated cardiovirulent coxsackievirus B3: The 5′‐nontranslated region does not contain major attenuation determinants

“…These data suggest that a carrier state was established in HDF cells, with a low level of replication of rCVB3 and lower infectivity titre of the virus compatible with previous observations [Ginsberg, 1958,19801. Interestingly, this noncytolytic, carrier state is similar to CVB3 infection of murine neonatal skin fibroblasts (MNSF) or fibroblast cultures prepared from heart tissue of CD-1 mice either 10-14 days or 4-6 weeks old [Lutton and Gauntt, 19861. Similarly, CVB3-infected human foetal myocardial fibroblasts produced virus continuously for 6-9 months after surviving, implying a possible role in virus persistence in the heart after the initial infection [Kandolf et al, 19851. Carrier-state infection in nonpermissive cells such as HDF might be due to low expression of CVB3 receptors, which is essential to initiate infection by specific recognition and binding with virus, or to lack of host cell factors that allow viral replication and maximal biological synthesis [Andino et al, 19901. In the carrier-state CVB3 infection of MNSF cells mentioned above, particular surface changes have been confirmed by sequencing of p14V-1 genomic RNA.…”

Clinical and experimental aspects of viral myocarditis.

“…Whether lymphocytic effector cells directly mediate tissue injury or only produce lymphokines activating other inflammatory cells which actually lyse cardiocytes is not known. However, some circumstantial evidence favors the hypothesis that macrophages participate in lesion formation since activated rat macrophages have receptors for L-mannosyl or L-fucosyl residues (129,133) and murine heart tissues infected with a myocarditic variant of CVB3 express L-fucosyl residues as detected by lectin binding (82).…”

“…The new antigen, which reacts with the lectin Ulex europeaus agglutinin I, must contain carbohydrate elements. Since picornavirus proteins are not usually glycosylated, these investigators concluded that the new antigen must be of cellular origin and therefore represents a neoantigen (82). Subsequently, a CTL was isolated which reacts to new cellular antigens induced on cardiocytes when cellular metabolism, including RNA and protein syntheses, is inhibited (55a).…”