Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus.

Hantavirus cardiopulmonary syndrome is a zoonotic illness associated with a systemic inflammatory immune response, capillary leak, noncardiogenic pulmonary edema, and shock in humans. Cytokines, including TNF, IFN-gamma, and lymphotoxin, are thought to contribute to its pathogenesis. In contrast, infected rodent reservoirs of hantaviruses experience few or no pathologic changes and the host rodent can remain persistently infected for life.

Ribavirin, human convalescent plasma and anti-beta3 integrin antibody inhibit infection by Sin Nombre virus in the deer mouse model.

The New World hantavirus Sin Nombre virus (SNV) is an aetiological agent for the often-fatal hantavirus cardiopulmonary syndrome (HCPS). There is no disease model for SNV and specific treatments for HCPS do not exist. By using the deer mouse infectious model, the in vivo inhibitory potential of ribavirin, human anti-SNV immune plasma (HIP), an anti-beta3 antibody (ReoPro) and a polyclonal rabbit anti-recombinant nucleocapsid (N) antibody against SNV was investigated.

Use of IgG avidity to indirectly monitor epizootic transmission of sin nombre virus in deer mice (Peromyscus maniculatus).

An IgG avidity assay was developed to differentiate deer mice that had recently acquired Sin Nombre virus (SNV) from those that were infected in the distant past. Using this procedure, low avidity antibodies were predominantly detected in experimentally infected deer mice (89.5%) within the first 30 days post-inoculation.