Sonia Navas-Martin
Affiliations: | Drexel University College of Medicine, Philadelphia, PA, United States |
Area:
Microbiology Biology, Virology Biology, ImmunologyGoogle:
"Sonia Navas-Martin"
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Publications
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| Chen NC, Partridge AT, Tuzer F, et al. (2018) Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection. The Journals of Gerontology. Series a, Biological Sciences and Medical Sciences |
| Swaminathan G, Pascual D, Rival G, et al. (2014) Hepatitis C virus core protein enhances HIV-1 replication in human macrophages through TLR2, JNK, and MEK1/2-dependent upregulation of TNF-α and IL-6. Febs Letters. 588: 3501-10 |
| Swaminathan G, Martin-Garcia J, Navas-Martin S. (2013) RNA viruses and microRNAs: challenging discoveries for the 21st century. Physiological Genomics. 45: 1035-48 |
| Perales-Linares R, Navas-Martin S. (2013) Toll-like receptor 3 in viral pathogenesis: friend or foe? Immunology. 140: 153-67 |
| Gupta A, Swaminathan G, Martin-Garcia J, et al. (2012) MicroRNAs, hepatitis C virus, and HCV/HIV-1 co-infection: new insights in pathogenesis and therapy. Viruses. 4: 2485-513 |
| Mazaleuskaya L, Veltrop R, Ikpeze N, et al. (2012) Protective role of Toll-like Receptor 3-induced type I interferon in murine coronavirus infection of macrophages. Viruses. 4: 901-23 |
| Bouchard MJ, Navas-Martin S. (2011) Hepatitis B and C virus hepatocarcinogenesis: lessons learned and future challenges. Cancer Letters. 305: 123-43 |
| Rossi F, Querido B, Nimmagadda M, et al. (2008) The V1-V3 region of a brain-derived HIV-1 envelope glycoprotein determines macrophage tropism, low CD4 dependence, increased fusogenicity and altered sensitivity to entry inhibitors. Retrovirology. 5: 89 |
| Weiss SR, Navas-Martin S. (2005) Coronavirus pathogenesis and the emerging pathogen severe acute respiratory syndrome coronavirus. Microbiology and Molecular Biology Reviews : Mmbr. 69: 635-64 |
| Navas-Martin S, Hingley ST, Weiss SR. (2005) Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein. Journal of Virology. 79: 7629-40 |