B Cell Mediated Lysis of JHMV Infected Targets
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Humoral immunity has been implicated in various models of mouse hepatitis virus (MHV) central nervous system (CNS) infection (Stohlman, et al., 1999). However, the lack of neutralizing Ab until the virus has been cleared suggested that humoral immunity played little or no role in clearance of JHMV from the CNS. Infection of mice lacking the ability to produce Ab showed that following acute clearance, infectious virus reactivates within the CNS (Lin et al., 1999), demonstrating an essential role for humoral immunity in preventing CNS virus reactivation. The absence of both B cells and Ab in these mice leaves open the question of whether the B cells limit CNS virus reactivation, a role potentially masked by Ab mediated neutralization (Lin et al. 1999). B cells from naïve mice interact with MHV-A59 infected cells resulting in lysis (Holmes et al. 1986, Welsh et al. 1986). Lysis is blocked by neutralizing Ab (Wysocka et al. 1989), suggesting a role of the S protein. B cells, although resistant to MHV infection, express high levels of the MHV receptor (MHV-R) (Coutelier et al 1994). Interactions between the S protein and MHV-R appear to result in cytolysis via cell-cell fusion (Wysocka et al. 1989) and is independent of Fas/FasL interactions and TNF-α (Nishioka et al 1993). These studies were initiated to explore the potential role of B cell-MHV-R interactions in contributing to the suppression of infectious virus within the CNS.
KeywordsHumoral Immunity Infectious Virus Mouse Hepatitis Virus Cell Mediate Lysis Control HeLa
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