By S. Tanuma, D. Shiokawa (auth.), Prof. Dr. Y. Kuchino, Prof. Dr. W. E. G. Müller (eds.)

Apoptosis performs a crucial function within the rules of mobile proliferation. Disruption of this keep an eye on mechanism can cause severe human ailments corresponding to encephalomyelitis and melanoma. hence, knowing of the molecular mechanisms of apoptotic mobile demise should still result in primary advances within the treatment of those diseases.

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It seems reasonable that both Vrl and another as yet undetermined region of F eL V-C gp70 (these authors would consider Vr5 a prime candidate) contribute to anemia development (see also Hartke 1992). 1 , 1 6 Speculative Relationship to Endogenous Virus Recombinants and Importance Across Evolution Also of marked interest is the homology between the Vr5 region of the cytopathic FeLV-Cs with the endogenous Fe LV (enFeLV) pro viruses intrinsic to the cat genome. Recent studies by our laboratories and others have shown that enFeLv proviruses are widely expressed by feline hemolymphatic tissues in vivo and by feline lymphoid cells in vitro (McDougall et al.

Science 257: 217- 219 Miller MA, Montelaro RC (1992) Amphipathic helical segments of human immunodeficiency virus type I transmembrane proteins and their potential role in viral cytopathicity. In: Aloia RC (ed) Advances in membrane fluidity, Vol 6. Liss, New York, pp 351 - 364 Miller MA, Garry RF, Jaynes JM, Montelaro RC (1991) A structural correlation between lentivirus transmembrane proteins and natural cytolytic peptides. AIDS Res Hum Retrovir 7: 511 - 519 Miller MA, Cloyd MW, Liebmann J, Rinaldo CR Jr, Islam KR , Wang SZS, Mietzner TA, Montelaro RC (I 993a) Alterations in cell membrane permeability by the lentivirus lytic peptide (LLP-I) ofHIV-1 transmembrane protein.

L. Rojko et al. 34 picture of selective but not generalized immunosuppression in FeLV infection (reviewed in Rojko and Hardy 1994) and the ability of cytopathic FeL V isolates to induce programmed cell death/terminal differentiationlapoptosis in certain T-cell subsets in vitro and thymic atrophy in vivo. Induction of apoptosis in certain thymic precursor cells could result in the absence of some but not all T -cells and potentially create holes in the T-cell repertoire and the observed selective acquired immunodeficiency in FeLV-viremic cats.

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