Critical role for CD4(+) T cells in controlling retrovirus replication and spread in persistently infected mice.

Abstract:

:Reactivations of persistent viral infections pose a significant medical problem in immunocompromised cancer, transplant, and AIDS patients, yet little is known about how persistent viral infections are immunologically controlled. Here we describe a mouse model for investigating the role of the immune response in controlling a persistent retroviral infection. We demonstrate that, following recovery from acute Friend virus infection, a small number of B cells evade immunological destruction and harbor persistent virus. In vivo depletions of T-cell subsets in persistently infected mice revealed a critical role for CD4(+) T cells in controlling virus replication, spread to the erythroid lineage, and induction of erythroleukemia. The CD4(+) T-cell effect was independent of CD8(+) T cells and in some cases was also independent of virus-neutralizing antibody responses. Thus, the CD4(+) T cells may have had a direct antiviral effect. These results may have relevance for human immunodeficiency virus (HIV) infections where loss of CD4(+) T cells is associated with an increase in HIV replication, reactivation of persistent viruses, and a high incidence of virus-associated cancers.

journal_name

J Virol

journal_title

Journal of virology

authors

Hasenkrug KJ,Brooks DM,Dittmer U

doi

10.1128/JVI.72.8.6559-6564.1998

subject

Has Abstract

pub_date

1998-08-01 00:00:00

pages

6559-64

issue

8

eissn

0022-538X

issn

1098-5514

journal_volume

72

pub_type

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