
pmid: 15110529
We established a viral persistence model that involves the adoptive transfer of spleen cells from immunocompetent mice (H-2(d)) into Hantaan virus (HTNV)-infected severe combined immunodeficient (SCID, H-2(d)) mice. The infection is maintained despite the presence of neutralizing antibodies, without apparent signs of disease, and there is a correlation between HTNV persistence and the lack of HTNV-specific CD8(+) T cells. In addition, disseminated HTNV infection before the initiation of immune responses appears to be important for virus persistence. The suppression of HTNV-specific CD8(+) T cells in the present model appears to occur at the periphery. The present study also demonstrates that CD8(+) T cells contribute to the clearance of HTNV. Thus, it seems that HTNV-specific CD8(+) T cells play a key role in HTNV persistence in mice. This model of viral persistence is useful for studies of immune responses and immunocytotherapy against viral infection.
Cytotoxicity, Immunologic, Mice, Inbred BALB C, Viral Core Proteins, Adoptive transfer, Mice, Nude, Persistent infection, CD8-Positive T-Lymphocytes, Adoptive Transfer, Hantaan virus, Disease Models, Animal, Mice, SCID mice, Virology, Hemorrhagic Fever with Renal Syndrome, Chronic Disease, Animals, Humans, Capsid Proteins, CD8+ T cell, Hantavirus
Cytotoxicity, Immunologic, Mice, Inbred BALB C, Viral Core Proteins, Adoptive transfer, Mice, Nude, Persistent infection, CD8-Positive T-Lymphocytes, Adoptive Transfer, Hantaan virus, Disease Models, Animal, Mice, SCID mice, Virology, Hemorrhagic Fever with Renal Syndrome, Chronic Disease, Animals, Humans, Capsid Proteins, CD8+ T cell, Hantavirus
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