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* Division of Immunoregulation and
Division of Virology, Medical Research Council National Institute for Medical Research, London, United Kingdom;
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840
Although the adaptive immune response almost invariably fails to completely eliminate retroviral infections, it can exert significant protection from disease and long-term control of viral replication. Friend virus (FV), a mouse retrovirus, causes persistent infection in all strains of mice and erythroleukaemia in susceptible strains, the course of which can be strongly influenced by both genetic and extrinsic factors. In this study we examine the impact of coinfection on the requirements for immune control of FV infection. We show that congenic C57BL/6 mice, in which the introduction of an allele of the Friend virus susceptibility 2 gene provides the potential for FV-induced leukemia development, effectively resist FV infection, and both T cell- and Ab-dependent mechanisms contribute to their resistance. However, we further demonstrate that coinfection with lactate dehydrogenase-elevating virus (LDV) renders these otherwise immunocompetent mice highly susceptible to FV infection and subsequent disease. The presence of LDV delays induction of FV-specific neutralizing Abs and counteracts the protective contribution of adaptive immunity. Importantly, the disease-enhancing effect of LDV coinfection requires the presence of a polyclonal B cell repertoire and is reproduced by direct polyclonal B cell activation. Thus, immune activation by coinfecting pathogens or their products can contribute to the pathogenicity of retroviral infection.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the U.K.’s Medical Research Council and the Portuguese Foundation of Science and Technology (SFRH/BD/15208/2004 to I.A.).
2 Address correspondence and reprint requests to Dr. George Kassiotis, Division of Immunoregulation, Medical Research Council National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, U.K. E-mail address: gkassio{at}nimr.mrc.ac.uk
3 Abbreviations used in this paper: FV, Friend virus; F-MuLV, Friend helper murine leukemia virus; SFFV, spleen focus-forming virus; Fv2, Friend virus susceptibility 2; B6, C57BL/6; C, BALB/c; LDV, lactate dehydrogenase-elevating virus; HEL, hen-egg lysozyme; iu, infectious units; MA, matrix; SI, spleen index.
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