mTORC1 restricts hepatitis C virus RNA replication through ULK1-mediated suppression of miR-122 and facilitates post-replication events.

The mechanistic target of rapamycin (mTOR), an important kinase that assimilates several upstream signals, associates into two functional complexes, mTORC1 and mTORC2. In this study, we demonstrate that HCV infection activates mTORC1 that functions in important antiviral response. Pharmacological inhibition of mTOR complexes augmented cellular HCV RNA levels, the observation confirmed further by Raptor depletion, indicating antiviral roles of mTORC1.

HIV Tat protein: Is Tat-C much trickier than Tat-B?

Out of various subtypes of human immunodeficiency virus type 1 (HIV-1), subtype B and C cause most of the infections worldwide. Clade specific differences have been reported in differences in clinical picture of HIV pathogenesis. Transcription of the HIV-1 genome is regulated by the interaction of HIV Tat protein to the trans-activation response (TAR) element.