HIV: Current Research
Open Access

Immune System Response to HIV Co-Infected Patients

Thomas Juie^{* *}Correspondence: Thomas Juie, Department of Epidemiology, Harvard University, Boston, USA, Email:

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Description

Although research and drug development have advanced significantly since the first Human Immunodeficiency Virus (HIV) was discovered thirty years ago, an effective vaccine against HIV/AIDS is still unavailable. There are several challenges to be addressed, one of which being HIV's extraordinary ability to mutate and evade the body's defenses. It is thought that this integration of the virus's genetic material into the cellular genome during the life cycle enables the virus to elude the host's immunological defenses. HIV can so continue for months or even years. Moreover, immunological dysfunction brought on by HIV infection means that the host is unable to stop the virus from replicating.

Furthermore, active CD4+ T cells are the cells that HIV preferentially targets. In fact, resting CD4+ T cells are either nonpermissive for HIV or very mildly so, while other CD4+ cells, such macrophages, only produce trace amounts of virus particles. In contrast, activated CD4+ T cells generate enormous amounts of virus particles. The sign of HIV infection is a substantial and long-lasting rise in activated CD4+ T cells. Stated differently, HIV replicates and grows inside its own target cells. There are still a lot of unsolved questions. For instance, there is still disagreement over whether an AIDS vaccine should stimulate anti-HIV T cells, anti-HIV antibodies, or both; it is also unclear what characteristics effective anti-HIV T cells should have, as well as how and where antibodies must be created.

The lack of a vaccination has made alternate approaches increasingly crucial. Hopes for an HIV cure have increased due to recent advancements in the field. The International AIDS Society's "towards an HIV cure" project has set out several targets aimed at ending HIV infection or, in the event that antiretroviral medications are not available, achieving a long-term remission of infection during which the host can manage viral replication. However, it currently appears improbable that HIV will be eradicated in a sizable patient population. We are encouraged to think that HIV remission may be a goal by the natural models of AIDS control and the cases of individuals who are able to limit replication after treatment discontinuation.

The clinical course of HIV-1 infection is expected to be significantly influenced by the immunological response that occurs early in the infection. According to recent findings, the HIV-1 quasispecies that develop when a virus infects the mucosa typically originate from a single transmitted virus. Furthermore, understanding the early immune reactions to the transmitted virus and their roles in regulating acute viremia is made possible by the discovery that the selection of virus escape mutations is driven by the first effective immune responses. Subsequently, there are robust innate and adaptive immune responses, but it is too late to eradicate the infection. The quality and kinetics of early immune responses to HIV-1, as well as their implications for the development of a viable preventative vaccine, are covered in this review of recent research.

Though it appears robust, the T lymphocyte-mediated cellular immune response to the human immunodeficiency virus is unable to entirely eradicate the infection. T cells either eradicate the virus or keep it dormant as a harmless infection for an extended period of time in the majority of viral infections. However, this control is compromised by the human immunodeficiency virus, which infects important immune cells and reduces the ability of both infected CD4+ T cells and uninfected CD8+ T cells to respond. The latter's inability to operate effectively allows viruses to evade immune system control and ultimately leads to the immune system's collapse.