scholarly journals Emergence of CD134 cysteine-rich domain 2 (CRD2)-independent strains of feline immunodeficiency virus (FIV) is associated with disease progression in naturally infected cats

Retrovirology ◽  
2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Paweł M Bęczkowski ◽  
Navapon Techakriengkrai ◽  
Nicola Logan ◽  
Elizabeth McMonagle ◽  
Annette Litster ◽  
...  
2006 ◽  
Vol 80 (7) ◽  
pp. 3386-3394 ◽  
Author(s):  
Brian J. Willett ◽  
Elizabeth L. McMonagle ◽  
Susan Ridha ◽  
Margaret J. Hosie

ABSTRACT The feline homologue of CD134 (fCD134) is the primary binding receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD4+ helper T cells. However, with disease progression, the cell tropism of FIV broadens such that B cells and monocytes/macrophages become significant reservoirs of proviral DNA, suggesting that receptor utilization may alter with disease progression. We examined the receptor utilization of diverse strains of FIV and found that all strains tested utilized CD134 as the primary receptor. Using chimeric feline × human CD134 receptors, the primary determinant of receptor function was mapped to the first cysteine-rich domain (CRD1) of fCD134. For the PPR and B2542 strains, the replacement of CDR1 of fCD134 (amino acids 1 to 64) with human CD134 (hCD134) alone was sufficient to confer nearly optimal receptor function. However, evidence of differential utilization of CD134 was revealed, since strains GL8, CPGammer (CPG41), TM2, 0827, and NCSU1 required determinants in the region spanning amino acids 65 to 85, indicating that these strains may require a more stringent interaction for infection to proceed.


2006 ◽  
Vol 80 (15) ◽  
pp. 7744-7747 ◽  
Author(s):  
Brian J. Willett ◽  
Elizabeth L. McMonagle ◽  
Francesca Bonci ◽  
Mauro Pistello ◽  
Margaret J. Hosie

ABSTRACT The feline homologue of CD134 is the primary binding receptor for feline immunodeficiency virus (FIV), targeting the virus preferentially to activated CD4+ helper T cells. However, strains of FIV differ in utilization of CD134; the prototypic strain PPR requires a minimal determinant in the first cysteine-rich domain (CRD1) of feline CD134 to confer near-optimal receptor function, while strains such as GL8 require additional determinants in the CD134 CRD2. We map this determinant to a loop in CRD2 governing the interaction between the receptor and its ligand; the amino acid substitutions S78N-S79Y-K80E restored full viral receptor activity to the CDR2 of human CD134 in the context of feline CD134, with tyrosine-79 appearing to be the critical residue for restoration of receptor function.


2003 ◽  
Vol 77 (16) ◽  
pp. 8819-8830 ◽  
Author(s):  
Malou C. Gemeniano ◽  
Earl T. Sawai ◽  
Christian M. Leutenegger ◽  
Ellen E. Sparger

ABSTRACT The orf-A (orf-2) gene of feline immunodeficiency virus (FIV) is a small open reading frame predicted to encode a 77-amino-acid protein that contains putative domains similar to those of the ungulate lentiviral Tat protein. Orf-A is reported to be critical for efficient viral replication in vitro and in vivo. A series of FIV-pPPR-derived proviruses with in-frame deletions and point mutations within orf-A were constructed and tested for replication in feline lymphoid cells. Orf-A mutant proviruses were also tested for viral gene and protein expression, viral particle formation, and virion infectivity. Deletions within orf-A severely restricted FIV replication in feline peripheral blood mononuclear cells (PBMC) and interleukin-2-dependent T-cell lines. In addition, substitutions of alanines for leucines in the putative leucine-rich domain, for cysteines in the putative cysteine-rich domain, and for a tryptophan at position 43 in Orf-A restricted the replication of FIV mutants. Deletions and point mutations in orf-A imposed a small effect or no effect on FIV long-terminal-repeat-driven viral gene expression and had no effect on viral protein expression. However, release of cell-free, virion-associated viral RNA in supernatants from cells transfected with orf-A mutant proviruses was severely restricted but was rescued by cotransfection with a wild-type Orf-A expression vector. In addition, virions derived from orf-A mutant proviruses expressed reduced infectivity for feline PBMC. Our findings suggest that Orf-A functions involve multiple steps of the FIV life cycle including both virion formation and infectivity. Furthermore, these observations suggest that Orf-A represents an FIV-encoded analog more similar to the accessory gene vpr, vpu, or nef than to the regulatory gene tat encoded by the primate lentiviruses.


2000 ◽  
Vol 182 (3) ◽  
pp. 725-732 ◽  
Author(s):  
Margaret C. Barr ◽  
Jean‐Noel Billaud ◽  
Donald R. Selway ◽  
Salvador Huitron‐Resendiz ◽  
Kent G. Osborn ◽  
...  

2002 ◽  
Vol 76 (19) ◽  
pp. 10079-10083 ◽  
Author(s):  
Yuko Goto ◽  
Yoshiaki Nishimura ◽  
Kenji Baba ◽  
Takuya Mizuno ◽  
Yasuyuki Endo ◽  
...  

ABSTRACT We measured the quantity of plasma feline immunodeficiency virus (FIV) RNA using a real-time sequence detecting system. Plasma viral RNA load was shown to correlate with the clinical stage, survival time, and disease progression in naturally FIV-infected cats. The present study indicates that the plasma viral RNA load can be used as a clinical marker representing the impairment of the immune system and predicting the clinical outcome in FIV-infected cats.


1994 ◽  
Vol 68 (7) ◽  
pp. 4572-4579 ◽  
Author(s):  
F Baldinotti ◽  
D Matteucci ◽  
P Mazzetti ◽  
C Giannelli ◽  
P Bandecchi ◽  
...  

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