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Nanoemulsions: Status in Antimicrobial Therapy
Published in Adwitiya Sinha, Megha Rathi, Smart Healthcare Systems, 2019
Atinderpal Kaur, Rakhi Bansal, Sonal Gupta, Reema Gabrani, Shweta Dang
Acquired immunodeficiency syndrome (AIDS) is one of the deadliest epidemics in the world. Human immunodeficiency virus (HIV), a retrovirus, is the causative organism for AIDS (Rios, 2014). HIV mainly affects the host immune system, making the person more susceptible to opportunistic infectious diseases and tumors (Soares, Garbin, Moimaz, & Garbin, 2014). A vast majority of people suffering from AIDS belong to low- and middle-income countries. The antiretroviral therapy includes drugs in various class reverse transcriptase inhibitors nucleoside reverse transcriptase inhibitor (NRTI), nonnucleoside reverse transcriptase inhibitors (NNRTI), protease inhibitor (PI), and fusion inhibitors (FI). Highly active antiretroviral therapy includes a combination of two or more drugs in combinatory action (Chearskul, Rongkavilit, Al-Tatari, & Asmar, 2006). Despite many advances in antiretroviral therapy, there is still no cure for it. New approaches and efforts are needed to address the epidemic.
Anti-HIV Agents
Published in Mihai V. Putz, New Frontiers in Nanochemistry, 2020
The classes of therapeutical agents are: Entry inhibitors (fusion inhibitors) – EI.Reverse-transcriptase inhibitors (nucleoside analogs – NRTI, nonnucleoside analogs – NNRTI, and nucleotide analogs – NtRTI).Integrase inhibitors – INSTIs.Protease inhibitors – PI.Maturation inhibitors – MI.
Optimal control in a multi-pathways HIV-1 infection model: a comparison between mono-drug and multi-drug therapies
Published in International Journal of Control, 2021
Chittaranjan Mondal, Debadatta Adak, Nandadulal Bairagi
Antiretroviral therapy has been found successful to reduce the viral load significantly and to increase the cells count, thus preventing the onset of AIDS and increasing the life-span of HIV-1 infected patients. Although significant improvement in the management of viremia using antiretroviral drug therapies is possible, complete resolution of HIV-1 infection from the host body is yet to be achieved. Mainly two types of drugs are used to suppress HIV-1 infection in a host (Perelson & Ribeiro, 2013). Reverse transcriptase inhibitors block the synthesis of viral DNA from HIV-1 RNA and thereby reduces viral infectivity. On the other hand, protease inhibitors are used to inhibit the proper cleavage of viral polyprotein inside the infected cell and thereby reduces the number of functionally effective viral production. Different models have been proposed and studied taking into the effect of drug therapies (Fister, Lenhart, & McNally, 1998; Joshi, 2002; Kirschner, Lenhart, & Serbin, 1997; Nowak, Bonhoeffer, Shaw, & May, 1997; Orellana, 2009; Perelson & Nelson, 1999; Rong & Perelson, 2009; Wodarz & Nowak, 2002; Zhou, Liang, & Wu, 2014). These models consider spread of infection through a single pathway, which is cell-free mode. It is reported that cell-to-cell spread allows HIV-1 to overcome barriers to infection (Agosto et al., 2014; Carr, Hocking, Li, & Burrell, 1999; Chen et al., 2007). There are evidences that antiretroviral drugs like tenofovir (TFV), efavirenz (EFV) and zidovudine (AZT) show reduced effectiveness to inhibit cell-to-cell transmission (Agosto et al., 2014; Duncan, Russell, & Sattentau, 2013; Permanyer et al., 2012). Sigal et al. (2011) demonstrated that cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy. Observations of these studies suggest that existing antiretroviral drugs may be efficient to control cell-free transmission, but unable to inhibit the dissemination of infection through cell-to-cell mode. Recent study by Hübner et al. (2009), therefore, suggests that future control strategies through drug therapy and vaccination should focus on blocking the cell-to-cell dissemination of infection. Assuming the existence of a drug that inhibits cell-to-cell transmission, we here study the effect of different antiretroviral therapies and analyse the dynamics of the system in the presence of therapeutic controls. We want to test a panel of controls for their ability to decline virus count and to enhance the count of uninfected cells in the blood plasma of a hypothetical HIV-1 infected patient. We would vary each control separately to compare the controllability of each inhibitory drug. In particular, we want to verify whether the drug which is supposed to block cell-to-cell infection is a better option to control HIV-1 infection.