Disease-free mosquito bred to disease-carrier can have all disease-free progeny

bianjie submitted, created time 1 year 5 months (www.eurekalert.org)

Researchers from Virginia Tech and the University of California Irvine have demonstrated the ability to express a foreign gene exclusively in the female mosquito germline, a necessary prerequisite to future genetic control strategies in mosquitoes where all progeny of lab and wild mosquitoes will have the gene that blocks virus replication -- or whatever trait has been introduced into the lab mosquitoes.

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Anopheles gambiae heat shock protein cognate 70B impedes onyong-nyong virus replication.

captainclaw submitted, created time 1 year 5 months (www.biomedcentral.com)

"These results indicate that HSC70B plays important roles in homeostasis and suppression of ONNV replication in the vector, An. gambiae. Biological implications of these findings are that while mosquitoes allow ONNV to replicate in them, they also check viral titers so that ONNV infection will result in no harmful effect on mosquitoes. Therefore, mosquitoes can function as vectors of ONNV transmission to humans while ONNV infection in An. gambiae remains asymptomatic."

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Sequential structures provide insights into the fidelity of RNA replication

crackpot submitted, created time 1 year 7 months (www.pnas.org)

"RNA virus replication is an error-prone event caused by the low fidelity of viral RNA-dependent RNA polymerases. Replication fidelity can be decreased further by the use of mutagenic ribonucleoside analogs to a point where viral genetic information can no longer be maintained. For foot-and-mouth disease virus, the antiviral analogs ribavirin and 5-fluorouracil have been shown to be mutagenic, contributing to virus extinction through lethal mutagenesis

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Replication of hepatitis C virus

addict submitted, created time 1 year 7 months (www.nature.com)

Exciting progress has recently been made in understanding the replication of hepatitis C virus, a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma worldwide. The development of complete cell-culture systems should now enable the systematic dissection of the entire viral lifecycle, providing insights into the hitherto difficult-to-study early and late steps. These efforts have already translated into the identification of novel antiviral targets and the development of new therapeutic strategies, some of which are currently undergoing clinical evaluation.

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The Carboxy-Terminal Domain of Glycoprotein N of Human Cytomegalovirus Is Required for Virion Morphogenesis

crackpot submitted, created time 1 year 8 months (jvi.asm.org)

"Researchers have constructed a series of mutants in gN to study the function of this protein. gN of HCMV is a type I glycoprotein containing a short carboxy-terminal domain of 14 amino acids, including two cysteine residues directly adjacent to the predicted transmembrane anchor at positions 125 and 126. Deletion of the entire carboxy-terminal domain as well as substitution with the corresponding region from alpha herpesviruses or mutations of both cysteine residues resulted in a replication-incompetent virus

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Suppression of MicroRNA-Silencing Pathway by HIV-1 During Virus Replication

psychologist submitted, created time 1 year 9 months (www.sciencemag.org)

MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 19 to 25 nucleotides that function as gene regulators and as a host cell defense against both RNA and DNA viruses. This research provides miRNA-silencing machinery is playing a physiological roles in controlling HIV-1 replication. Type III RNAses Dicer and Drosha, responsible for miRNA processing, inhibited virus replication both in peripheral blood mononuclear cells from HIV-1–infected donors and in latently infected cells. In turn, HIV-1 actively suppressed the expression of the polycistronic miRNA cluster miR-17/92

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Influenza A Virus NS1 Protein Activates the PI3K/Akt Pathway To Mediate Antiapoptotic Signaling Responses

amanda submitted, created time 1 year 9 months (jvi.asm.org)

NS1 not only blocks but also activates signaling pathways to ensure efficient virus replication.

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