Host-regulating factors

Host-Regulating Factors Associated with Parasitic Hymenoptera... 

COVDRON Host-Regulating Factors and Paraskic Hymenoptera... 

Table I. Parasitic Hymenoptera With Host-Regulating Factors ...

COUDRON Host-Regulating Factors and Parasitic Hymeno era... 

Coudron, T.A., 1991. Host-regulating factors associated with parasitic Hymenoptera. ACS Symp. Ser. 449 41-65. 

Fig. 5.1 Regulators of pre- and post-integration latency. Pre-integration latency is regulated as the viral RNA is reverse transcribed into the proviral DNA (A). This is controlled by the avaUabdity of the nucleotide pool, half life of the forming proviral cDNA copy, and the interaction of the viral protein Vif with the cellular antiviral protein APOBEC, espedaUy family members 3G and 3R It is also regulated at the step of transport across the nuclear membrane through the availability of ATP as the process requires energy (B). Post-integration, the proviral DNA copy of the viral genome, is regulated maiiily by the avadabdity of host transcription factors, especially NF-kB and NFAT (C)...

Thus, viral- and host-specific factors regulate the frequency of HSE. 

Strack, A., Schluter, D., Asensio, V. C., Campbell, I. L., and Deckert, M. (2002). Regulation of the kinetics of intracerebral chemokine gene expression in murine Toxoplasma encephalitis Impact of host genetic factors. Glia 40, 372-377. 

This model is compatible with our findings with the temperature-sensitive MSV-NRK cell line. In these cells, the hypothetical repressor would be a heat-labile protein. Unfortunately, there are not yet any mouse cells transformed by a temperature-sensitive virus available to further explore this hypothesis. This model does not readily explain the flat revertant cell lines. Analogous to bacterial systems, one would expect such a repressor molecule to be dominant. However, the existence of these flat revertants indicates that host cell factors are involved in the expression of the transformed phenotype. Little is known about the regulation of glycolipid synthesis, but undoubtedly cellular control mechanisms do exist. It is conceivable that a viral gene product could interfere with the normal regulation and biosynthesis of these compounds. Such a mechanism could explain the elevated levels of other glycosyltransferases. Impaired feedback control could result in continual expression of these enzyme activities. 

Hematopoietic (blood) cells transport oxygen and carbon dioxide, contribute to host immunity, and facilitate blood clotting [1], A complex, interrelated, and multistep process, called hematopoiesis, controls the production as well as the development of specific marrow cells from immature precursor cells to functional mature blood cells. This well-regulated process also allows for replacement of cells lost through daily physiologic activities. The proliferation of precursor cells, the maturation of these into mature cells, and the survival of hematopoietic cells require the presence of specific growth factors. 

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