By Yechiel Becker (auth.), Yechiel Becker, Gholamreza Darai (eds.)
The reports during this targeted factor of VIRUS GENES supply details at the mechanisms wherein viruses have advanced including their common hosts via buying RNA and DNA molecules from the contaminated cells into their genomes. half A is dedicated to stories on virus genes that have been got to stay away from the vertebrate host immune approach. half B bargains with the purchase of mobile and international virus genes via Herpes and Irido viruses. The reviews offered partially C describe the poxvirus genes which are homologues of mobile genes. jointly, those reports offer an perception into the evolutionary techniques that viruses have built to manage the metabolic equipment of the contaminated tissue cells, and to avoid the security equipment of the contaminated host, e.g., the immune method, from spotting the infecting virus. Such mechanisms might clarify the pathogenicity and mirror the virulence of viruses.
Molecular Evolution of Viruses - prior and current: Evolution ofViruses by way of Acquisition of mobile RNA and DNA used to be preceded through VIRUS GENES specific matters at the evolution of viruses (VIRUS GENES 11:2/3, 1996, and VIRUS GENES 16:1, 1998). the 1st distinctive factor handled the evolution of retrons, retroelements, retroviruses and endogenous retroviruses and present evolution of viruses. the second one distinctive factor supplied details at the evolution of human, marine algae and fungal viruses. those concerns, including the 3rd designated factor on virus evolution, offer an attractive perception into the evolution of DNA and RNA viruses.
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Extra info for Molecular Evolution of Viruses — Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA
IRLGFLLMCALPT .......... D ........... PK .... TLLSLSPRQQ ... V MRIQ ... DL .......... QYR .. REFVKRQLAPK ... S MRRW ... LRLLVGLGCCWVTLAHAGNPYEDDDYYYYREDE .......... SKSVRLPQYPRGFGDVSGYRVSSSVSE MLR ...... LRNPLAI .......... CLLWWLG . . . . . . . . . . . VVAAATEE ...... TREPTYFTCG MNL .... VMLILALWAPVAG ...... SMPELSLTLF .. DE .......... PP .... QCLQAAKKRP ..... KTHKSRPNDRNLEGRLTCQRVR .. RLLPCDLD ..... IHPS. CVIDGG ... IASEVILHDT ..... SGLYNVPHEIQ .. NDGQVLTVTVKRSAPADIAKVLISLKP .. CVVKDG ...
4b show that US2-. US6- and USll-transfectants display a drastically reduced MHC class I surface density compared to untransfected control cells. Exposure of cells to graded concentrations of IFN-y increases MHC class I expression in untransfected control cells in a dose-dependent order. The IFN-y effect is reproduced in the presence of MHC 1subversive HCMV gene functions, albeit to an extent depending on the US gene expressed (Fig. 4A,B). After stimulation with IFN-y. a surplus of MHC I molecules escapes from the control by the viral inhibitors and reaches the cell surface, where few MHC I molecules suffice for CTL recognition.
DIERLLFEDRRLMAYYALTIKSAQYTLMMVAVIQV ... FWGLYVKGWL ... HR US6 US7 USB US9 USIa USII 178 210 217 234 182 207 · IRRCGS ......... FTGKPTYNLLTYPVKG CVPQKCEKSLC ..... ATGRTSREEEAKDD .. PPRE ........... HFPWMFSDQW ...... Fig. 2. Amino acid sequence alignment of the US2 family members US2 and US3 (A) and the US6 family members US6 through US]] (B). Numbers indicate the amino acid positions within the published amino acid sequences (1). Amino acids identical in more than 50% of the genes arc highlighted.