Feline immunodeficiency virus

Johnston JB, SUva C, Power C (2002) Envelope gene-mediated neurovirulence in feline immunodeficiency virus infection induction of matrix metalloproteinases and neuronal injury. J Virol 76 2622-2633... 

PMEA and its congeners are more effective in vivo than could be predicted from their in vitro potency. While less potent as an antiretrovirus agent than AZT in vitro, PMEA proved clearly superior to AZT when the two drugs were compared for their effectiveness in vivo, in mice infected with murine Moloney sarcoma virus [51,52]. PMEA was also shown to be effective against various other retrovirus infections, including Friend leukemia virus (FLV), Rauscher leukemia virus (RLV), and LP-BM5 (murine AIDS) virus infection in mice, feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV) infection in cats, and SIV infection in macaque (rhesus) monkeys (for review, see Ref. 53). In the latter model [54], again PMEA proved far superior to AZT in suppressing several parameters of the disease. 

Barr, M. et al., Effects of multiple acute morphine exposures on feline immunodeficiency virus disease progression, J. Infect. Dis., 182, 725, 2000. 

Barr, M. et al., Escalating morphine exposures followed by withdrawal in feline immunodeficiency virus-infected cats A model for HIV infection in chronic opiate abusers, Drug Alcohol Depend.., 72, 141, 2005. 

There is no good animal model for infection by HIV. The virus will infect several primates, but it does not produce active disease and it is not practical to use primates for propagation of the virus. The chimpanzee has been used in vaccine trials to determine whether neutralizing antibody is produced and whether the growth of the virus can be inhibited in vivo. More productive work has been done using the immunodeficiency viruses of the species (e.g., simian immunodeficiency virus in macaques, feline immunodeficiency virus in cats) to study pathogenesis and treatment of retroviral acquired immunodeficiencies. 

Next, it was determined whether the same active regions of IFN- were involved in additional systems. The Type I IFN receptor on cells has been reported to be somewhat more promiscuous than on other cell types [16] therefore, vesicular stomatitis challenge of Fc-9 cells was performed. Only the carboxy-terminal peptide inhibited IFN- activity in this system [17]. This suggested that it was the carboxy-terminus that was crucial to receptor interaction. In studies examining IFN-T-treated feline immunodeficiency virus infected FeT-1 cells and human immunodeficiency virus-infected peripheral... 

Chen, H., Mcbroom, D.G., Zhu, Y.Q., Gold, L. and North, T.W. (1996) Inhibitory RNA ligand to reverse transcriptase from feline immunodeficiency virus. Biochemistry, 35, 6923-6930. 

Otero, G.C., Harris, ME., Donello, J.E. and Hope, T.J. (1998) Leptomycin B inhibits equine infectious anemia virus Rev and feline immunodeficiency virus rev function but not the function of the hepatitis B virus posttranscriptional... 

A newer generation of retroviral vectors, based on the lentivirus, hold the same advantages of retroviral vectors with the added ability to transduce non-dividing cells efficiently. Pre-clinical studies with lentiviral vectors for the treatment of hemophilia have shown great promise. Using a feline immunodeficiency virus (FlV)-based vector, Stein et al. showed that 9 of 12 treated hemophilia A mice could express greater than 5 ng/ml factor VIII, six of which... 

DN double/dominant negative FIV feline immunodeficiency virus... 

Beebe AM, Dua N, Faidr TG, Moore PE, Pederserr NC, Darrdekar S (1994) Primary stage of feline immunodeficiency virus hrfecdorr Viral dissemirradon and cellular targets. J Virol 68 3080—3091. 

Bragg DC, Childers TA, Tompkirrs MB, Tompkhrs WA, Meeker RB (2002) hrfecdorr of dre choroid plexus by feline immunodeficiency virus. JNeurovirol 8 211—224. 

English RV, Jolmson CM, Gebhai d DH, Tompkins MB (1993) In vivo lymphocyte dopism of feline immunodeficiency virus. J Virol 67 5175-5186. 

Hein A, Schuh H, Thiel S, Martin IP, Domes R (2003) Ramified feline microglia selects for distinct variants of feline immunodeficiency virus during early central nervous system infection. I Neurovirol 9 465 76. 

Hurti el M, Ganiere IP, Guelfi IF, Chaki abairi L, Maire MA, Gray F, Montagnier L, Hurti el B (1992) Compaiison of eai ly and late feline immunodeficiency virus encephalopatliies. AIDS 6 399 06. 

Power C, Buist R, Johnston JB, Del Bigio MR, Ni W, Dawood MR, Peeling J (1998) Neurovirulence in feline immunodeficiency virus-infected neonatal cats is viral sti ain specific and dependent on systemic immune suppression. J Virol 72 9109-9115. 

Steffan AM, Lafon ME, Gendrault JL, Koehren F, De Monte M, Royer C, Kirn A, Gut JP (1994) Feline immunodeficiency virus can produedvely infect cultured endothelial cells fiom cat brain microvessels. J Gen Virol 75(Pt 12) 3647—3653. 

Retroviruses encode a protease (PR) responsible for cleaving polyprotein precursors, and such processing is essential for proper virion assembly and maturation. Based on the presence of a sequence Asp-Ser/Thr-Gly in the active sites of retroviral proteases (1) and their inhibition in vitro by pepstatin (2-7), these enzymes have been classified as members of the aspartic protease family. Crystal structures have been determined for the proteases from Rous sarcoma virus (RSV PR) (8), from two variants and several mutants of the human immunodeficiency vims (HIV PR) (9-11), from feline immunodeficiency virus (FIV PR) (12) and from equine infectious anemia vims (EIAV PR) (13). Aspartic proteases contain a single active site which includes two aspartates. In apoenzymes, the two catalytic Asp residues from the active site triad have been found to be in hydrogen bond contact with a water molecule (10). Mutations of the active site Asp25 in HIV-1 PR into Asn (14,15), Thr (3) or Ala (4,16,17) led to an inactive enzyme. Similarly, the RSV PR was inactivated by mutation of its active site Asp to He (18). 

Dow SW, Poss ML, Hoover EA (1990) Feline immunodeficiency virus A neurotropic lentivirus. J Acquir Immune Defic Syndr 3 658-668. 

English RV, Nelson P, Johnson CM, Nasisse M, Tompkins WA, Tompkins MB (1994) Development of clinical disease in cats experimentally infected with feline immunodeficiency virus. J Infect Dis 170 543-552. 

Johnston JB, Power C (2002) Feline immunodeficiency virus xenoin-fection The role of chemokine receptors and envelope diversity. J Virol 76 3626-3636. 

Steigerwald ES, Sarter M, March P, Podell M (1999) Effects of feline immunodeficiency virus on cognition and behavioral function in cats. J Acquir Immune Defic Syndr Hum Retrovirol 20 411-419. 

Willett BJ, Hosie MJ (1999) The role of the chemokine receptor CXCR4 in infection with feline immunodeficiency virus. Mol Membr Biol 16 67-72. 

SrV) and feline immunodeficiency virus (FIV), respectively, but studies with these viruses have not provided a clear indication of the influence of opioids on the development of these immunodeficiency diseases. In one smdy, monkeys maintained on morphine had a slower progression of SIV infection, although temporary withdrawal augmented viral load (Donahoe et al., 1993), but in another, their progression was more rapid (Chuang et al., 1997). Neither acute nor chronic morphine or withdrawal altered FTV infection in cats, but the number of animals was small and the variance in FTV load large (Barr et al., 2003). 

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