Junin Virus Infection in Genetically Athymic Mice

Abstract

The progression of Junin virus infection was studied in congenitally athymic mice. Immunocompetent littermates were used as infected controls. As expected, the latter developed lethal encephalitis, with viremia and considerable viral replication in the brain. The mortality rate was almost 100%; the few surviving controls exhibited high serum neutralizing antibody levels and a total absence of virus in blood and brain. In contrast, nude mice did not contract the disease; all survived with persistent viremia and virus in brain, but no serum neutralizing antibodies were detected. These results confirm previous research on thymectomized mice and those treated with anti-lymphocyte serum and tend to support the important role of cellular immunity in the pathogenesis of this viral disease.

Induction of Junin Virus Persistence in Adult Athymic Mice

“…A deficient immune response probably enables esta blishment and perhaps maintenance of virus persistence [1]. In this connection, newborn athymic (nu/nu) mice infected with Junin virus have been a useful model to study the role of T cells in the development of patho genesis as well as virus clearance [2,3], In the case of lymphocytic choriomeningitis (LCM) virus, infection of nude mice usually pro duces high viremia, although clinical signs are absent and complement-fixing serum antibodies (Abs) fail to develop [4].…”

“…However, in nu/nu newborn mice, Junin vi rus replicates but induces persistent central nervous system (CNS) infection with high viremia, and animals survive without neuro logic illness [2].…”

“…Previous work on newborn immuno competent mice has demonstrated that both neurologic disease and virus clearance are mediated by thymus-dependent lympho cytes; the absence of cell response precludes disease and leads to virus persistence without Abs, as shown in nude [2], thymectomized [6], and antithymocyte serum-treated mice [10].…”

“…Because anti-Junin Abs failed to develop in virus-infected nude mice, either in adults, as shown in this paper, in suckling mice [2] or after antithymocyte serum treatment of im munocompetent adults [7], it is suggested that Junin virus behaves as a thymus-dependent antigen. In further support, LCM virus, the prototype member of Arenaviridae, also has been shown to behave as a thymus-depend ent antigen [13].…”

Nonhuman Transferrin Receptor 1 Is an Efficient Cell Entry Receptor for Ocozocoautla de Espinosa Virus

“…TfR1 seems to be the primary cell entry receptor for these viruses (7), but TfR1-independent replication has been observed in vitro, as well as in certain laboratory-mouse models (8)(9)(10)(11)(12). Importantly, human TfR1 is utilized only by the pathogenic clade B viruses but not by nonpathogenic AMAV or TCRV (13,14).…”