Special Issue "Viruses and miRNAs"

Guest Editor
Prof. Dr. Andrew P. Rice
Nancy Chang Professor, Rice Lab - Molecular Virology & Microbiology, One Baylor Plaza, Mail Stop BCM-385, Houston, Texas 77030, USA
Website: http://www.bcm.edu/molvir/ricelab/?pmid=18017
E-Mail: arice@bcm.edu
Phone: 713-798-5774

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Type of Paper: Review
Title: MicroRNAs and Hepatitis C Virus: New Insights in Pathogenesis and Therapy
Authors: Archana Gupta ^1,2,  Gokul Swaminathan ^1,2, Julio Martin-Garcia ^2,3, and Sonia Navas-Martin ^2,3*
Affiliation: ¹Microbiology and Immunology Graduate Program; ²Department of Microbiology and Immunology, ³Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA
E-Mails: ag434@drexel.edu (A.G.); gs337@drexel.edu (G.S.); julio.martin-garcia@drexelmed.edu (J.M.G.); sonia.navas-martin@drexelmed.edu (S.N.M.);
* Author to whom correspondence should be addressed; Tel: +1 215 762 7284, Fax: + 1 215 762 8284, sonia.navas-martin@drexelmed.edu
Abstract: MicroRNAs (miRNAs) can exert a profound effect on HCV replication. The interaction of HCV with the highly liver-specific miRNA, miR-122 represents one such unique example of viruses having evolved mechanism(s) to usurp the host miRNA machinery to support viral life cycle. Furthermore, HCV infection can also trigger changes in the cellular miRNA profile which may ultimately contribute to the outcome of viral infection. Various HCV proteins have been implicated in mediating such effects through direct interaction with components of the RNA interference (RNAi) pathway. Accumulating knowledge on HCV- host miRNA interactions has ultimately influenced the design of therapeutic interventions against chronic HCV infection.
Keywords: microRNA, mir-122, HCV, hepatitis C virus, hepatitis, antiviral response, HIV-HCV coinfection, antagomir, therapeutics

Type of Paper: Article
Title: MicroRNAs in Resting Cells and HIV-1 Restriction
Authors: Karen Chiang ^{1, 2} and Andrew P. Rice ^{1, 2}
Affiliations: ¹Department of Molecular Virology & Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA
²Interdepartmental Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, TX, 77030, USA
Abstract: In contrast to activated CD4⁺ T cells and differentiated macrophages, resting CD4⁺ T cells and monocytes are non-permissive for HIV-1 replication.  The mediators which regulate the resting phenotype are often actively involved in the restriction of viral replication and the establishment and maintenance of viral latency.  Recently, certain microRNAs which are highly expressed in resting cells have been implicated in this capacity, inhibiting the expression of cellular proteins that are also viral co-factors; following activation these microRNAs exhibit decreased expression, while their targets are correspondingly up-regulated, contributing to a favorable milieu for virus replication.   Other microRNAs exhibiting a similar expression pattern in resting and activated cells have been shown to directly target the HIV-1 genome.  In this review we will discuss the resting state and the causes behind viral restriction in resting cells, with emphasis on the role of microRNAs.

Type of Paper: Review
Tentative Title: EBV and KSHV miRNAs
Author: Joseph M. Ziegelbauer
Affiliation: National Cancer Institute, HIV and AIDS Malignancy Branch, Building 10, Room 6N110, NCI-Bethesda, Bethesda, MD 20892; Phone: 301-594-6634; http://ccr.cancer.gov/staff/staff.asp?profileid=15171; E-Mail: ziegelbauerjm@mail.nih.gov
Abstract: Herpesviruses are unique amongst other DNA viruses due to their ability to encode for multiple miRNA genes.  In the gamma-herpesvirus family, EBV and KSHV share many similarities like their association with proliferative diseases, B cell tropism, and genomic regions with clustered microRNA genes. Surprisingly, there is no significant sequence homology between EBV- and KSHV- encoded microRNAs. However, recent evidence from microRNA-associated protein immunoprecipitation and deep sequencing experiments have suggested that the majority of EBV and KSHV microRNA targets are shared between the two viruses. Early evidence suggests different microRNAs bind to distinct regions of the same mRNA targets. Here we explore the similarities in functions of validated and predicted viral microRNA targets to elucidate common themes in viral microRNA functions