Viral genome copies integrate into the genome of memory T cells (CD4+ T cells) and remain invisible to the immune system [51, 52]. Induction of transcription in these cells leads to the formation of infectious viral particles [53]. The development of an anti-HIV-1 vaccine is considered as an alternative option. Currently, several fundamentally new approaches to HIV-1 treatment are under development, including the use of neutralizing antibodies, genome editing, and blocking an integrated latent provirus. This review explains a traditional approach involving HIV-1 inhibitors as well as the prospects of other treatment options. CXCR4 shows the approved anti-HIV drug cocktails used in HAART. Table 2 Drug combinations (cocktails) used in complex treatment of a HIV contamination thead th rowspan=”1″ colspan=”1″ Combination /th th rowspan=”1″ colspan=”1″ Trade name /th th rowspan=”1″ colspan=”1″ FDA approval /th /thead Lamivudine/Zidovudine (3TC/ZDV)Combivir27/9/1997Abacavir/Lamivudine/Zidovudine (ABC/3TC/ZDV)Trizivir14/11/2000Abacavir/Lamivudine (ABC/3TC)Epzicom2/8/2004Emtricitabine/Tenofovir (FTC/TDF)Truvada2/8/2004Efavirenz/Emtricitabine/Tenofovir (EFV/FTC/TDF)Atripla12/6/2006Emtricitabine/Rilpivirine/Tenofovir (FTC/RPV/TDF)Complera10/8/2011 Elvitegravir/Cobicistat/Emtricitabine/Tenofovir K+ Channel inhibitor br / (QUAD, EVG/COBI/FTC/TDF) Stribild27/8/2012Abacavir/Dolutegravir/Lamivudine (ABC/DTG/3TC)Triumeq22/8/2014Atazanavir/Cobicistat (ATV/COBI)Evotaz29/1/2015Darunavir/Cobicistat (DRV/COBI)Prezcobix29/1/2015 Elvitegravir/Cobicistat/Emtricitabine/Tenofovir/Alafenamide br / (EVG/COBI/FTC/TAF) Genvoya5/11/2015 Open in a separate window OTHER APPROACHES TO THE TREATMENT OF HIV-1 INFECTION Over the past 25 years, the attention of researchers has focused primarily for the optimization and development of drugs to K+ Channel inhibitor suppress HIV-1 replication. The antiviral treatment that’s utilized, including HAART, offers its limitations. Individuals have to consider medicines throughout their lives, BMP2 while fresh mutant types of the disease emerge that are resistant to an array of medicines. Upon long-term therapy, the medicines may cause a cumulative toxic effect. Many industry experts agree a fresh approach must enable K+ Channel inhibitor the accomplishment of long term remission under milder treatment circumstances. Also, life routine inhibitors suppress HIV-1 just in cells with energetic viral replication, however they do not influence a latent disease. Viral genome copies integrate in to the genome of memory space T cells (Compact disc4+ T cells) and stay invisible towards the disease fighting capability [51, 52]. Induction of transcription in these cells qualified prospects to the forming of infectious viral contaminants [53]. The introduction of an anti-HIV-1 vaccine is recognized as an alternative choice. The 1st vaccine originated in the first 2000s; however, the potency of vaccination was lower than that of traditional anti- HIV medicines [54, 55]. Presently, the experience of so-called broad-spectrum neutralizing antibodies can be undergoing clinical tests. The full total outcomes of initial research claim that neutralizing antibodies could become guaranteeing anti-HIV medicines [56, 57]. Currently, the chance of influencing a K+ Channel inhibitor latent disease is being looked into. You can find two approaches, known as sterilizing and practical treatment. The sterilizing treatment means full purging of your body from the viral genome through the damage of cells bearing the provirus built-into their genome; the functional remedy can be an entire suppression of viral activity in the physical body, which includes obstructing latent provirus reactivation. Among the variants from the sterilizing treatment may be the transplantation of bone tissue marrow from donors resistant to the HIV disease (e.g., whose genome contains a mutant gene of HIV-1 co-receptors, 32 CCR5). As demonstrated in ’09 2009, this process enabled an entire treatment from the HIV disease; i.e., all copies from the viral genome were eliminated through the physical body. This event was known as the Berlin affected person [58]. The individual underwent radiation bone and therapy marrow transplantation from a donor with 32 CCR5. Later on, after discontinuation of anti- HIV therapy, the virus could no be detected his body. Initially, the entire case engendered great optimism among physicians. But to day, there were cases where this process has not got the desired impact. Therefore, the seek out other therapies proceeds. Latent provirus reactivation Among the sterilizing treatment variants may be the awakening of latent proviruses. Theoretically, medicine that’s in a position to reactivate a latent provirus can induce the transcription from the HIV-1 genome successively, synthesis of viral protein, and introduction of infectious HIV-1 contaminants, which would bring about the death from the contaminated cell and reduce the amount of latent HIV-1 copies in the human being genome. This process was called surprise and destroy. Cells holding viral genome copies are intended either to perish because of the cytopathic viral impact or to become destroyed from the immune system. This method should be coupled with maintenance therapy by HIV-1 inhibitors to avoid the spread K+ Channel inhibitor from the reactivated disease. Vorinostat, the histone deacetylase inhibitor found in tumor therapy, was researched like a potential anti-HIV-1 medication [59]. As was proven in cells produced from individuals and in medical tests, the inhibitor can induce the transcription of viral genes in a few individuals. At the same time, vorinostat can be cytotoxic and inadequate in every complete instances, making its wide medical application problematic. Additional histone deacetylase inhibitors are going through clinical tests [60, 61]. This process offers at least two drawbacks. The foremost is the side effects by means of nonspecific induction of sponsor cell gene transcription. The second reason is the impossibility to forecast whether all of the cells harboring induced proviruses perish. There is proof that the disease fighting capability cannot recognize each one of these cells [62]. Improvement with this path depends on developing a solution to destroy cells that harbor the activated provirus effectively. Combined with the investigation of.