Two different mutations in the envelope protein of feline immunodeficiency virus allow the virus to escape from neutralization by feline serum antibodies

https://doi.org/10.1016/0165-2427(94)07005-RGet rights and content

Abstract

Viral progeny of two molecular clones of feline immunodeficiency virus (FIV), 19k1 and 19k32, were tested in a virus neutralization assay. In this assay the infection of thymocytes with FIV 19k1 was neutralized by serum S1422, derived from an SPF cat 22 weeks after infection with FIV 19k1. We previously reported that a point mutation at position 560 in hypervariable region-5 (HV-5) of 19k1 confers resistance to virus neutralization (Siebelink et al., 1993, J. Virol. 67: 2202–2208). Viral progeny of the other molecular clone, FIV19k32, which differs in the envelope protein in only six amino acids from 19k1, was not neutralized. In order to map sites involved in virus neutralization we constructed chimeric clones by reciprocal exchange of 19k1 and 19k32 envelope gene fragments. Reciprocal exchange of a 1662 bp fragment, encoding almost the whole surface protein, which differs in five amino acids between these two clones, resulted in exchange of the phenotype. Amino acids of the envelope protein of 19k1 and 19k32, in which these clones differ, were substituted by point mutation. We demonstrated that one of these mutations, a substitution of leucine to serine at position 483 in HV-4, also conferred resistance of 19k1 to neutralization by serum S1422.

References (19)

There are more references available in the full text version of this article.

Cited by (11)

  • Mutations in the feline immunodeficiency virus envelope glycoprotein confer resistance to a dominant-negative fragment of Tsg101 by enhancing infectivity and cell-to-cell virus transmission

    2014, Biochimica et Biophysica Acta - Biomembranes
    Citation Excerpt :

    We had initially speculated the acquisition of TSG-5′-resistance by mutation of FIV Env (K410N) in the V3 loop would possibly affect virion binding affinity to CXCR4 and HSPGs, either positively or negatively, based on the reported correlations between overall net charge in this region and coreceptor affinity [65,90]. It has been shown that the net charge in the V3 loop differs between lab-adapted isolates grown in cell culture and primary isolates obtained from infected cats, which is actively maintained by selective pressures in both environments [68–70,91]. Since our study focused on FIV replication mediated by CD134-independent entry, the selection for resistance may have favored mutations in the HSPG or CXCR4-binding regions of FIV Env that are more highly utilized by the 34TF10 molecular clone.

View all citing articles on Scopus
View full text