Mechanisms Of HIV Infection Research Articles

CRISPR-Cas9 potential in treating HIV/AIDS

In this review paper, the mechanism of HIV infection and some of the most efficacious and updated gene therapy methods developed by scientists will be discussed in detail. Different editing strategy using the CRISPR-Cas9 system inhibits different times of the HIV life cycle are involved with all the same target, which is to block the HIV infection pathway as well as its own replication&proliferation pathway. As the most popular and promising way of treating different kinds of diseases which seemed to be incurable in the past, and CRISPR-Cas9 shows high potency under the data of experiments and clinical studies. These give scientists many confidence to run out more research on this new treatment for diseases and at the same time to improve and optimize the function and efficiency of this gene editing toolkit making sure it can used widely in the future as an actual clinical treatment for the HIV/AIDS.

Mechanisms of HIV infection, replication, latency, and/or pathogenesis and SUDs (NIDA)

Mechanisms of HIV infection, replication, latency, and/or pathogenesis and SUDs (NIDA)

Anatomical and physiological aspects of the HIV infection pathogenesis in animal models

Understanding the entire pathogenesis of HIV infection, from penetration at the gates of infection to the induction of severe immunodeficiency, is an essential tool for the development of new treatment methods. Less than 40 years of research into the mechanisms of HIV infection that lead to the development of acquired immunodeficiency syndrome have accumulated a huge amount of information, but HIV's own unique variability identifies new whitespaces.
 Despite the constant improvement of the protocols of antiretroviral therapy and the success of its use, it has not yet been possible to stop the spread of HIV infection. The development of new protocols and the testing of new groups of antiretroviral drugs is possible, first of all, due to the improvement of animal models of the HIV infection pathogenesis. Their relevance, undoubtedly increases, but still depends on specific research tasks, since none of the in vivo models can comprehensively simulate the mechanism of the infection pathology in humans which leads to multi-organ damage.
 The aim of the review was to provide up-to-date information on known animal models of HIV infection, focusing on the method of their infection and anatomical, physiological and pathological features.

Astrocytes as an HIV Reservoir: Mechanism of HIV Infection.

If we have any hope of achieving a cure for HIV infection, close attention to the cell types capable of getting infected with HIV is necessary. Of these cell types, astrocytes are the most ideal cell type for the formation of such a reservoir. These are long-lived cells with a very low turnover rate and are found in the brain and the gastrointestinal tract. Although astrocytes are evidently resistant to infection of cell-free HIV in vitro, these cells are efficiently infected via cell-tocell contact by which immature HIV virions bud off lymphocytes and have the ability to directly bind to CXCR4, triggering the process of fusion in the absence of CD4. In this review, we closely examine the evidence for HIV infection of astrocytes in the brain and the mechanisms for viral entry and regulation in this cell type, and discuss an approach for controlling this viral reservoir.

Nonlinear mixed-effects HIV dynamic models with considering left-censored measurements

HIV dynamic model offers a different perspective of studying HIV pathogenesis and developing treatment strategies for AIDS patients. Many HIV dynamic models have recently been developed to characterize short-term AIDS treatment, whereas in long-term HIV dynamics, viral load often rebounds in the later stage of treatment primarily due to reduced drug efficacy. Although time-varying drug efficacy can be incorporated into the ordinary differential equations (ODE) model, such a system has no analytical solution, and the measurement of viral load is usually censored at the detection limit due to technological constraints. We consider nonlinear mixed-effects ODE model with stochastic approximation EM algorithm to overcome these difficulties. The performance of the proposed method is illustrated by means of a simulation study and a real-data application. Numerical evidence shows that the HIV infection is generally more severe when considering left-censored data. The T cell production rate from human body source varies, but the death rate of infected T cells, infection rate of virus, and other dynamic parameters do not have much difference among patients. We hope these findings inspire more research on clarifying biological mechanism of HIV infection and developing better treatment.

High-affinity glycopolymer binding to human DC-SIGN and disruption of DC-SIGN interactions with HIV envelope glycoprotein.

Noncovalent interactions between complex carbohydrates and proteins drive many fundamental processes within biological systems, including human immunity. In this report we aimed to investigate the potential of mannose-containing glycopolymers to interact with human DC-SIGN and the ability of these glycopolymers to inhibit the interactions between DC-SIGN and the HIV envelope glycoprotein gp120. We used a library of glycopolymers that are prepared via combination of copper-mediated living radical polymerization and azide−alkyne [3+2] Huisgen cycloaddition reaction. We demonstrate that a relatively simple glycopolymer can effectively prevent the interactions between a human dendritic cell associated lectin (DC-SIGN) and the viral envelope glycoprotein gp120. This approach may give rise to novel insights into the mechanisms of HIV infection and provide potential new therapeutics.

Is RNA-laden p24 capsid protein a vector for HIV?

The consensus HIV infection pathway, although well supported by abundant experimental evidence, fails to account for infection of cells (e.g., neurons) that lack CD4 and/or coreceptors. We present the hypothesis that p24 capsid protein laden with RNA may be an alternative virulent agent. A novel mechanism of HIV infection may involve binding of the capsid with membrane receptors, followed by internalization of the capsid–receptor complex. This new pathway suggests novel strategies for antiviral pharmacotherapy.

The study of long-term HIV dynamics using semi-parametric non-linear mixed-effects models.

Modelling HIV dynamics has played an important role in understanding the pathogenesis of HIV infection in the past several years. Non-linear parametric models, derived from the mechanisms of HIV infection and drug action, have been used to fit short-term clinical data from AIDS clinical trials. However, it is found that the parametric models may not be adequate to fit long-term HIV dynamic data. To preserve the meaningful interpretation of the short-term HIV dynamic models as well as to characterize the long-term dynamics, we introduce a class of semi-parametric non-linear mixed-effects (NLME) models. The models are non-linear in population characteristics (fixed effects) and individual variations (random effects), both of which are modelled semi-parametrically. A basis-based approach is proposed to fit the models, which transforms a general semi-parametric NLME model into a set of standard parametric NLME models, indexed by the bases used. The bases that we employ are natural cubic splines for easy implementation. The resulting standard NLME models are low-dimensional and easy to solve. Statistical inferences that include testing parametric against semi-parametric mixed-effects are investigated. Innovative bootstrap procedures are developed for simulating the empirical distributions of the test statistics. Small-scale simulation and bootstrap studies show that our bootstrap procedures work well. The proposed approach and procedures are applied to long-term HIV dynamic data from an AIDS clinical study.

The Mechanism of HIV Infection and AIDS Development

The Mechanism of HIV Infection and AIDS Development

Biological function of H1V-1 transmembrane protein gp41

Since 1992, the study of biological functions of HIV-1 gp41 has made great progress. Experimental evidence from several research groups demonstrated that gp41 has a putative cellular receptor. A recombinant soluble gp41 (aa539–684) and gp41 immunosuppressive peptide (aa583–599) could bind to human B lymphocytes and monocytes, but weakly bind to T lymphocytes. It was found that gp41 contains two cellular binding sites (aa583–599 and 641–675). GP41 could selectively inhibit cell proliferation of human T, B lymphocytes and monocytes, enhance human MHC class I, II and ICAM-1 molecule expression on cell surface. Gp41 binding proteins and a monoclonal antibody against the first binding site could inhibit this modulation effect. Amino acid sequence homology exists between gp41 and human type I interferons, and the homologous region is located in the first binding site on gp41 and in the receptor binding site on type I interferons. Studies in other groups indicate that both binding sites in gp41 may be associated with HIV infection of cells. Peptides containing two binding sites could respectively inhibit HIV infection of cells. A monoclonal antibody recognizing the second binding site could neutralize lab-strains and recently separated strains of HIV-1. Besides, antibodies against two regions (homologous with gp41 binding sites) of SIV transmembrane protein gp32 could protect macaques from SIV infection. These results suggest that the study of gp41 binding sites and cellular receptor could contribute to understanding the mechanism of HIV infection and to developing HIV vaccine and anti-HIV drugs.

Developmental differences in knowledge of drugs and AIDS

Children 5 to 18 years of age, some with exposure to the drug culture, were interviewed about the drugs that drug users take, methods of drug use, and mechanisms of HIV infection. Although young children were surprisingly familiar with cocaine, they has many misconceptions about which forms of drug use cause AIDS. Knowledge of street drugs increased with age, and boys knew more drug terms than girls. Experiential factors also influenced understanding: Members of a small sample of adolescent drug users were especially knowledgeable about drugs, and children of drug users in treatment were especially informed about drugs in relation to AIDS. However, more important than gender, ethnicity, parent education, and drug-related experience, was age, possibly because it is associated with both cognitive growth and the accumulation of information.

The Mechanism of HIV Infection in Patients of the Florida Dentist-Reply

In Reply. —We do not believe that five patients of a Florida dentist became infected with HIV as a consequence of exposure to the sweat of a dentist with AIDS. 1-3 None of the five infected patients reported any contact with perspiration from the dentist. Furthermore, HIV has not been demonstrated in natural eccrine sweat from HIV-infected patients, 4 nor is there evidence to indicate that hepatitis B virus, another bloodborne pathogen with epidemiologic transmission patterns similar to HIV, can be transmitted through this route. Although the precise mode of HIV transmission to these patients remains uncertain, all of the patients had dental care from the dentist after he was diagnosed with AIDS, and multiple opportunities existed for the dentist to sustain needlestick injuries (eg, during administration of local anesthetics, two-handed needle recapping procedures, and suturing) or cuts with a sharp instrument, particularly in poorly visualized operative sites. Alternatively, transmission

The mechanism of HIV infection in patients of the Florida dentist

The mechanism of HIV infection in patients of the Florida dentist

Does HIV Cause AIDS?

AIDS is an acquired immunodeficiency syndrome caused by the lentivirus HIV and characterized by a successive depletion of CD4 helper/inductor lymphocytes. The humoral and cellular immune deficiency is the basis for the development of opportunistic infections and tumors. Because of a multitude of different bacterial, viral, and parasitic opportunistic agents, AIDS is typified by a number of divergent clinical symptoms. As with many lentiviruses, HIV is difficult to demonstrate in the organism, especially in asymptomatic carriers. Although the rate of infection in peripheral lymphocytes appears to be low, there is an increasing amount of virological and immunological data which help to explain the slow but irreversible failure of the immune defense. We still know relatively little about the pathogenic mechanisms of HIV, although a number of the presently available experimental results provide useful starting points for subsequent investigations. Peter H. Duesberg recently published that HIV and AIDS may well be correlated, but stated that HIV is not the cause of AIDS. Duesberg bases his hypothesis on the fact that HIV fulfills neither Koch's classic postulates nor several more of his own postulates for viral pathogenesis. Following the summary of individual pathogenic mechanisms of HIV infection, the separate points of Duesberg's hypothesis are discussed in detail. It is made very clear that the magnitude of epidemiologic, clinical, and experimental observations and results argue for a causal role of HIV and AIDS.

エイズウイルスの感染機構

エイズウイルスの感染機構