ABSTRACT
The HIV/AIDS epidemic in Russia is among the fastest growing in the world. HIV epidemic burden is non-uniform in different Russian regions and diverse key populations. An explosive epidemic has been documented among people who inject drugs (PWID) starting from the mid-1990s, whereas presently, the majority of new infections are linked to sexual transmission. Nationwide, HIV sub-subtype A6 (previously called AFSU) predominates, with the increasing presence of other subtypes, namely subtype B and CRF063_02A. This study explores HIV subtype B sequences from St. Petersburg, collected from 2006 to 2020, in order to phylogenetically investigate and characterize transmission clusters, focusing on their evolutionary dynamics and potential for further growth, along with a socio-demographic analysis of the available metadata. In total, 54% (107/198) of analyzed subtype B sequences were found grouped in 17 clusters, with four transmission clusters with the number of sequences above 10. Using Bayesian MCMC inference, tMRCA of HIV-1 subtype B was estimated to be around 1986 (95% HPD 1984-1991), whereas the estimated temporal origin for the four large clusters was found to be more recent, between 2001 and 2005. The results of our study imply a complex pattern of the epidemic spread of HIV subtype B in St. Petersburg, Russia, still in the exponential growth phase, and in connection to the men who have sex with men (MSM) transmission, providing a useful insight needed for the design of public health priorities and interventions.
Subject(s)
HIV Infections , HIV-1 , Sexual and Gender Minorities , Male , Humans , Homosexuality, Male , HIV Infections/epidemiology , HIV-1/genetics , Bayes Theorem , Russia/epidemiology , PhylogenyABSTRACT
Molecular studies suggest that HIV arose in Africa between 1880 and 1940. During this period, there were campaigns by European colonial governments that involved unsterile injections of large numbers of Africans. That, along with other unsafe therapeutic interventions, may have propelled the evolution of HIV from SIV. Since subtype B in Africa may have been concentrated in white African homosexuals, it is possible that Westerners rather than Haitians introduced the virus to the New World. Amplification of HIV subtype B took place in Haiti, where transmission was facilitated by hazardous medical procedures including plasmapheresis. Representations in the media, however, largely ignore Western contributions to the spread of AIDS. This article focuses on the value of alternative narratives in fostering a balanced view that is less stigmatizing on developing nations.
Subject(s)
Colonialism , Developing Countries , HIV Infections/etiology , HIV Infections/transmission , Health Services/standards , Iatrogenic Disease , Africa South of the Sahara , Blood Transfusion , Cuba , Equipment Contamination , Europe , Evolution, Molecular , Female , HIV-1/genetics , Haiti , Health Services/statistics & numerical data , Humans , Male , Sexual Behavior , Simian Immunodeficiency Virus/geneticsABSTRACT
Human immune virus subtype C is the most widely spread HIV subtype in Sub-Sahara Africa and South Africa. A profound structural insight on finding potential lead compounds is therefore necessary for drug discovery. The focus of this study is to rationalize the nine Food and Drugs Administration (FDA) HIV antiviral drugs complexed to subtype B and C-SA PR using ONIOM approach. To achieve this, an integrated two-layered ONIOM model was used to optimize the geometrics of the FDA approved HIV-1 PR inhibitors for subtype B. In our hybrid ONIOM model, the HIV-1 PR inhibitors as well as the ASP 25/25' catalytic active residues were treated at high level quantum mechanics (QM) theory using B3LYP/6-31G(d), and the remaining HIV PR residues were considered using the AMBER force field. The experimental binding energies of the PR inhibitors were compared to the ONIOM calculated results. The theoretical binding free energies (?Gbind) for subtype B follow a similar trend to the experimental results, with one exemption. The computational model was less suitable for C-SA PR. Analysis of the results provided valuable information about the shortcomings of this approach. Future studies will focus on the improvement of the computational model by considering explicit water molecules in the active pocket. We believe that this approach has the potential to provide much improved binding energies for complex enzyme drug interactions.