Equine infectious anemia virus (EIAV) is morphologically, genetically, and serologically related to human immunodeficiency virus (HIV) and thus provides a useful model for the study of virus-host interactions in lentivirus-induced disease. Characteristic of equine infectious anemia (EIA) is the episodic nature of clinical disease which is associated with the appearance of novel viral variants. This project is concerned with elucidating the factors important in the generation and selection of these viral variants and in understanding the role of variation in lentivirus persistence and pathogenesis. Our previous work suggested that early in the course of disease, EIAV variants may be selected in vivo by non-immunological mechanisms. We have therefore initiated studies on the in vitro host cell tropism of various strains of EIAV and its possible correlation with viral pathogenicity. Virus isolated which were selected for in vitro replication in continuous cell lines demonstrated a 1,000-10,000- fold reduction in viral replication in primary horse monocyte cultures (HMC) as compared to replication in continuous cell lines. Moreover, this marked reduction of viral replication in horse monocytes, believed to be the target cell for EIAV replication in vivo, was associated with a loss of viral virulence. This suggest that levels of viral replication in in vitro HMC may be a correlate of in vivo pathogenicity. Thus, we have increased our efforts to isolate a replication-competent molecular clone of EIAV which could serve as a basis for understanding structural viral features important in viral pathogenicity.
