http://www.mdpi.com/journal/viruses/special_issues/hiv-drug-resistance/ Submission Information All papers should be submitted to viruses@mdpi.org. To be published continuously until the deadline and papers will be listed together at the special issue website. Submitted papers should not have been published nor be under consideration for publication elsewhere. All papers are refereed through a peer-review process. A guide for authors is available on the Instructions for Authors page. Viruses is a new international, peer-reviewed, quarterly open access journal published by Molecular Diversity Preservation International. Article Processing Charges (APC) for publication in this Open Access journal are waived for well-prepared manuscripts submitted by 30 June 2010. English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections. http://www.mdpi.com/1999-4915/2/2/503/ Most of the current knowledge on antiretroviral (ARV) drug development and resistance is based on the study of subtype B of HIV-1, which only accounts for 10% of the worldwide HIV infections. Cumulative evidence has emerged that different HIV types, groups and subtypes harbor distinct biological properties, including the response and susceptibility to ARV. Recent laboratory and clinical data highlighting such disparities are summarized in this review. Variations in drug susceptibility, in the emergence and selection of specific drug resistance mutations, in viral replicative capacity and in the dynamics of resistance acquisition under ARV selective pressure are discussed. Clinical responses to ARV therapy and associated confounding factors are also analyzed in the context of infections by distinct HIV genetic variants. http://www.mdpi.com/1999-4915/2/2/503/ Tue, 02 Feb 2010 00:00:00 CET Viruses 2010-02-02 2 2 Review 503 531 1999-4915 HIV Genetic Diversity and Drug Resistance 2010-02-02 doi: 10.3390/v2020503 André F. Santos Marcelo A. Soares http://www.mdpi.com/1999-4915/2/2/372/ Nucleoside reverse transcriptase (RT) inhibitors of HIV block viral replication through the ability of HIV RT to incorporate chain-terminating nucleotide analogs during viral DNA synthesis. Once incorporated, the chain-terminating residue must be removed before DNA synthesis can continue. Removal can be accomplished by the excision activity of HIV RT, which catalyzes the transfer of the 3'-terminal residue on the blocked DNA chain to an acceptor substrate, probably ATP in most infected cells. Mutations of RT that enhance excision activity are the most common cause of resistance to 3'-azido-3'-deoxythymidine (AZT) and exhibit low-level cross-resistance to most other nucleoside RT inhibitors. The resistance to AZT is suppressed by a number of additional mutations in RT, most of which were identified because they conferred resistance to other RT inhibitors. Here we review current understanding of the biochemical mechanisms responsible for increased or decreased excision activity due to these mutations. http://www.mdpi.com/1999-4915/2/2/372/ Thu, 28 Jan 2010 00:00:00 CET Viruses 2010-01-28 2 2 Review 372 394 1999-4915 The Role of Nucleotide Excision by Reverse Transcriptase in HIV Drug Resistance 2010-01-28 doi: 10.3390/v2020372 Antonio J. Acosta-Hoyos Walter A. Scott