PMID- 9094660 OWN - NLM STAT- MEDLINE DCOM- 19970425 LR - 20200724 IS - 0022-538X (Print) IS - 1098-5514 (Electronic) IS - 0022-538X (Linking) VI - 71 IP - 5 DP - 1997 May TI - Maturation of the cellular and humoral immune responses to persistent infection in horses by equine infectious anemia virus is a complex and lengthy process. PG - 3840-52 AB - Equine infectious anemia virus (EIAV) provides a natural model system by which immunological control of lentivirus infections may be studied. To date, no detailed study addressing in parallel both the humoral and cellular immune responses induced in horses upon infection by EIAV has been conducted. Therefore, we initiated the first comprehensive characterization of the cellular and humoral immune responses during clinical progression from chronic disease to inapparent stages of EIAV infection. Using new analyses of antibody avidity and antibody epitope conformation dependence that had not been previously employed in this system, we observed that the humoral immune response to EIAV required a 6- to 8-month period in which to fully mature. During this time frame, EIAV-specific antibody evolved gradually from a population characterized by low-avidity, nonneutralizing, and predominantly linear epitope specificity to an antibody population with an avidity of moderate to high levels, neutralizing activity, and predominantly conformational epitope specificity. Analyses of the cell-mediated immune response to EIAV revealed CD4+ and CD8+ major histocompatibility complex-restricted, EIAV-specific cytotoxic T-lymphocyte (CTL) activity apparent within 3 to 4 weeks postinfection, temporally correlating with the resolution of the primary viremia. After resolution of the initial viremia, EIAV-specific CTL activity differed greatly among the experimentally infected ponies, with some animals having readily detectable CTL activity while others had little measurable CTL activity. Thus, in contrast to the initial viremia, it appeared that no single immune parameter correlated with the resolution of further viremic episodes. Instead, immune control of EIAV infection during the clinically inapparent stage of infection appears to rely on a complex combination of immune system mechanisms to suppress viral replication that effectively functions only after the immune system has evolved to a fully mature state 6 to 8 months postinfection. These findings strongly imply the necessity for candidate EIAV and other lentivirus vaccines to achieve this immune system maturation for efficacious immunological control of lentivirus challenge. FAU - Hammond, S A AU - Hammond SA AD - Department of Molecular Genetics and Biochemistry, School of Medicine, University of Pittsburgh, Pennsylvania 15261, USA. FAU - Cook, S J AU - Cook SJ FAU - Lichtenstein, D L AU - Lichtenstein DL FAU - Issel, C J AU - Issel CJ FAU - Montelaro, R C AU - Montelaro RC LA - eng GR - 5RO1 AI25810/AI/NIAID NIH HHS/United States GR - 5T32 AI07487/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - J Virol JT - Journal of virology JID - 0113724 RN - 0 (Antibodies, Viral) RN - 0 (Immunoglobulin G) SB - IM MH - Animals MH - Antibodies, Viral/*blood MH - Antibody Affinity MH - CD4-Positive T-Lymphocytes/immunology MH - Equine Infectious Anemia/*immunology MH - Horses MH - Immunoglobulin G/blood MH - *Lymphocyte Activation MH - Major Histocompatibility Complex MH - Protein Conformation MH - T-Lymphocytes, Cytotoxic/immunology PMC - PMC191535 EDAT- 1997/05/01 00:00 MHDA- 1997/05/01 00:01 PMCR- 1997/05/01 CRDT- 1997/05/01 00:00 PHST- 1997/05/01 00:00 [pubmed] PHST- 1997/05/01 00:01 [medline] PHST- 1997/05/01 00:00 [entrez] PHST- 1997/05/01 00:00 [pmc-release] AID - 10.1128/JVI.71.5.3840-3852.1997 [doi] PST - ppublish SO - J Virol. 1997 May;71(5):3840-52. doi: 10.1128/JVI.71.5.3840-3852.1997.