Research LettersLack of T-cell proliferative response to HIV-1 antigens after 1 year of highly active antiretroviral treatment in early HIV-1 disease
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Cited by (108)
Consensus Statement by GeSIDA/National AIDS Plan Secretariat on antiretroviral treatment in adults infected by the human immunodeficiency virus (Updated January 2013)
2013, Enfermedades Infecciosas y Microbiologia ClinicaEngineered DNA modifying enzymes: Components of a future strategy to cure HIV/AIDS
2013, Antiviral ResearchCitation Excerpt :Particularly, long-term treatment frequently results in secondary complications, such as diabetes, hyperlipidemia, cardiovascular disease, osteoporosis, and chronic kidney disease (Calmy et al., 2009; Deeks and Phillips, 2009). More importantly, patients successfully treated with ART for several years still do not fully recover their immune responses, and show increased levels of immune activation along with its harmful effects (Ostrowski, 2010; Plana et al., 1998). Consequently, low-level viral replication may persist along with an established pool of latently infected cells (Finzi et al., 1997, 1999; Palmer et al., 2008).
Consensus document of Gesida and Spanish Secretariat for the National Plan on AIDS (SPNS) regarding combined antiretroviral treatment in adults infected by the human immunodeficiency virus (January 2012)
2012, Enfermedades Infecciosas y Microbiologia ClinicaChallenges in dendritic cells-based therapeutic vaccination in HIV-1 infection. Workshop in dendritic cell-based vaccine clinical trials in HIV-1
2011, VaccineCitation Excerpt :There is increasing evidence that a strong HIV-1-specific CD4+ helper T-cell response is crucial in order to achieve a sustained and effective HIV-1-specific CD8+ cytotoxic T-lymphocyte (CTL) response able to control HIV-1 replication both in the macaque model [10] and in humans [5,11,12] and this concept is entirely consistent with recent data on chronic viral infections in the mouse model [13]. Although HIV-1-specific CD8 T-cells and CD4 T-cells secreting interferon gamma (IFN-gamma) can be found in most HIV-1-infected individuals, the CD4 T-cell proliferative response is absent [4,6,12] and the cytolytic activity of CD8 T-cells is defective [14–16]. Some data suggest that the antigen presenting cell (APC) functions of dendritic cells (DC) are also impaired in HIV-1-infected patients and this could contribute to dysfunction in HIV-1-specific helper and CTL responses [17–19].
Ex vivo production of autologous whole inactivated HIV-1 for clinical use in therapeutic vaccines
2011, VaccineCitation Excerpt :Combined antiretroviral therapy (cART) inhibits HIV-1 replication to levels below the limit of detection of standard clinical assays, allowing the restoration of normal or nearly normal CD4 T cell counts and protective T cell immunity to opportunistic pathogens in most patients, and has dramatically reduced the morbidity and mortality of HIV-1 infection. However, in spite of these clinical benefits, cART is incapable of eradicating HIV-1, and also fails to restore HIV-specific T cell responses able to durably and effectively to control HIV-1 replication when antiretroviral drugs are discontinued [1–5]. Thus, cART must be administered for life, increasing the risk of drug-related adverse effects, the potential for emergence of drug resistant mutant viral variants, along with some inconvenience for the patients and economic burden for the patient and society [6,7].
National Consensus Document by GESIDA/National Aids Plan on Antiretroviral Treatment in Adults Infected by the Human Immunodeficiency Virus (January 2011 Update)
2011, Enfermedades Infecciosas y Microbiologia Clinica