Nature 1970, 227:680–685.CrossRefPubMed 20. Whiting Jl, Rostenm PM, Chow AW: Determination by Western blot (immunoblot) of seroconversions

to Toxic Shock Syndrome (TSS) Toxin 1 and enterotoxin A, B, or C during infection with TSS- and Non- TSS-associated Staphylococcus aureus. Infect Immu 1989, 57:231–234. Authors’ contributions MN carried out the molecular genetic studies, participated in the sequence alignment, performed the immunoassays and drafted the manuscript. KY prepared the anti TSST-1 antibody. AO participated in the sequence alignment. TH participated in the design of C188-9 the study. YH and MO conceived the study and participated in its design and coordination. All PARP inhibitor Authors read and approved the final manuscript.”
“Background Arthropod-borne viruses (arboviruses) such as Sindbis and Chikungunya viruses are transmitted to humans through the bite of an infected mosquito. The viruses exhibit significant morbidity

and mortality in the vertebrate host. However, virus persists in the mosquito vector with minimal associated pathology. Examples of arbovirus-induced cytopathology during infection have been described with laboratory-infected mosquitoes, but little is known about the interplay between virus and vector that allows for sustainable arbovirus infection in the environment [1–5]. The persistent nature of arbovirus infection of a vector suggests a commensal rather than parasitic relationship. A factor of particular interest in this relationship is the interaction of viral replication QVDOph and the mosquito RNA interference (RNAi) response to infection. RNAi is a highly conserved Dehydratase molecular pathway triggered by the presence of intracytoplasmic double-stranded RNA (dsRNA)

that results in the cleavage of RNA molecules with sequence homologous to the dsRNA. In insects, RNAi is a major antiviral pathway that modulates arbovirus infection. Keene et al (2004) and Campbell et al (2008) used dsRNA injection to show that transient knockdown of key RNAi components increases viral loads in individual mosquitoes. Titers of O’nyong-nyong virus (ONNV) in Anopheles gambiae and Sindbis virus in Aedes aegypti were higher if Argonaute-2 or Dicer-2 expression was silenced [6, 7]. These studies show that RNAi restricts replication of an arbovirus in the mosquito. During replication of the alphavirus genome, positive- and negative-sense RNAs form dsRNA intermediates that could be recognized and cleaved by Dicer-2. Alternatively, secondary structure of the positive-sense RNA genome may be targeted by the RNAi machinery, as was shown in plants infected with positive-sense, ssRNA viruses [8, 9]. SINV-specific siRNAs of both polarities have been detected in infected mosquitoes with increased sense siRNAs being observed [6, 10], suggesting secondary structure is the primary, but not only, molecular RNAi trigger. Thus SINV replication appears to be targeted by the RNAi response in mosquitoes.