Miguel Angel Martínez

I am the Principal Investigator of the IrsiCaixa HIV and HCV Genetic and Phenotypic Variability group. I obtained in 1989 a PhD in Biological Sciences from the Universidad Autónoma de Madrid (UAM), followed by a Postdoctoral fellowship from the European Commission that allowed me to specialize in HIV/AIDS at the Pasteur Institute (Paris) for 3 years. I joined IrsiCaixa (Barcelona) in 1997 and since then I have co-authored more than 100 papers, four worldwide patents and have supervised 12 doctoral theses. I am Editor of Antimicrobial Agents and Chemotherapy (American Society for Microbiology, ASM), Assistant Editor of Frontiers in Microbiology and member of the Editorial Board of Antiviral Research (International Society for Antiviral Research, ISAR). I am also the author of eleven book chapters and guest editor of the book ” RNA Interference and Viruses, Current Innovations and Future Trends”, Caister Academic Press. Norfolk, UK, 2010. I have been for more than 10 years (2003-2014) the head of the Virology section of the Catalan Biology Society. In 2006 the International AIDS Society (IAS) gave me the award of the most highly cited author in basic science of the AIDS Journal. My research group is interested in the genetic variability of HIV-1 HCV. The study of viral variation can promote the design of new antiviral strategies that take into account the high mutability of HIV-1 and HCV. In search of new alternative antiviral strategies for HIV-1, we have applied a new methodology which allows recode and synthesize parts of the virus genome in such a way to preserve its wild-type amino acid sequence and producing an attenuation of virulence. This can be achieved by creating suboptimal patterns of codon or codon-pair usage, and/or CpG/UpA dinucleotide frequencies. This technique has been used to generate attenuated virus vaccines for poliovirus, influenza, Chikungunya virus, human respiratory syncytial virus, porcine reproductive and respiratory syndrome virus, echovirus 7, tick-borne encephalitis virus, vesicular stomatitis virus, dengue virus and HIV-1. Deoptimizing different moieties of the HIV-1 genes has allowed us to generate HIV-1 variants with attenuated phenotypes. Synonymous virus genome recoding can also aid in investigating virus interactions with innate immune responses, identifying functional virus genome structures, strategically ameliorating cis-inhibitory signaling sequences related to complex viral functions, to unravel the relevance of codon usage for the temporal regulation of viral gene expression and improving our knowledge of virus mutational robustness and adaptability. The frequency of liver fibrosis markers is high in patients infected with HIV-1 and it is associated with high morbidity and mortality. Particularly severe are the effects caused by HCV co-infection because these patients have higher rates of liver decompensation than patients mono-infected with HCV. Our research group have identified a repertoire of 1425 micro(mi)RNAs in the plasma of patients infected with HIV-1, of which, 193 had their level of expression altered, depending on the presence of co-infection with HCV, high transaminases, focal nodular hyperplasia or liver fibrosis. The importance of the function and distribution of miRNAs in diverse cellular processes and the recent evidences of their role in communication between cells makes us hypothesize that circulating miRNAs predict and/or indicate liver disease progression. The probable direct involvement of these miRNAs in pathological processes also makes them possible new therapeutic targets. Since the beginning of the COVID-19 pandemic, and due to our previous experience with SARS-CoV, we are planning to search for possible antivirals against this new coronavirus.