Work in the Lane laboratory is currently divided into three broad areas:

1) Defining the functional role of host factors that contribute to defense and disease following viral infection of the central nervous system (CNS)

2) Evaluating strategies to promote remyelination in response to viral-induced demyelination

3) Discerning the effects of SARS-CoV-2 infection on the CNS in the context of Alzheimer’s disease

To accomplish these goals, we use intracranial (i.c.) inoculation of susceptible mice with the neuroadapted JHM strain of mouse hepatitis virus (JHMV, a positive-sense RNA virus member of the Coronaviridae family), and this results in an acute encephalomyelitis, characterized by viral replication in astrocytes, microglia and oligodendroglia, with relative sparing of neurons. Virus-specific CD4+ and CD8+ T cells control viral replication through secretion of IFN-γ and cytolytic activity, respectively. Sterile immunity is not acquired, and virus persists in white matter tracts of surviving mice that ultimately develop an immune-mediated demyelinating disease with clinical and histologic characteristics similar to the human demyelinating disease, multiple sclerosis (MS).