Hiv Virus In Humans And Its Life Cycle Biology Essay

Human immunodeficiency virus ( HIV ) is a lentivirus belonging to household Reteroviidae and was identified in early 1980s. Members of this household are responsible for doing assorted immunological and neurological diseases in worlds and animate beings. Acquired immune lack syndrome ( AIDS ) is caused by HIV. AIDS is a status in which the immune system of host Begins to neglect and finally leads to life endangering infections. HIV is an endemic infection that can be transferred by organic structure fluids such as blood transfusion, seeds, vaginal fluids, and chest milk and from an septic female parent to child during birth.

Life rhythm of HIV

HIV infection is caused by a figure of controlled stairss. Entry is one of the stairss by which viral interaction with cellular membrane of host cell occurs. This interaction causes the deposition of HIV-1 genome in the mark host cell. Membrane enclosed viruses can come in the host cells by two ways, pH-dependent endocytosis and direct interaction with the plasma membrane of the host cell. Entry of HIV is of import to understand for the development of drugs in more beforehand manner to handle the persons infected with HIV-1.

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Encapsidation of viral RNA genome, release of virus atoms and their assembly is driven by Gag proteins. There are three pol encoded enzymes peptidase ( PR ) , rearward RNA polymerase ( RT ) and integrase ( IN ) . Gag Pol polyprotein precursors and Gag are cleaved by these enzymes at the clip of absolution of virus atoms. Hp68, a cellular protein reinforces the procedure of virus assembly. This cleavage causes the viral RNA genome to change over into dual stranded Deoxyribonucleic acid. Integration of viral DNA into the host cell chromosome is promoted by this procedure. These viral encoded proteins actively take the advantage from the host cell for viral scattering. CD4 cells provide receptor for the binding of viral proteins. But entirely CD4 cells are non responsible for HIV-1 infection. There are seven membrane connected G proteins holding chemokine receptors promotes the binding of HIV-1 to CD4 receptor for facilitation of membrane merger. Cholesterol rich lipid tonss of host cell facilitate the entry of virus for the reproduction rhythm. Recruitment and concentrations of merger reaction are associated with these lipid tonss by making lipid microenvironment that shows compatibility with the merger reaction. Another part of lipid tonss is to advance flight of septic cells. HIV-1 Gag protein interacts with lipid tonss to enfeeble the production of HIV-1 atoms.

Rearward RNA polymerase

Infectivity of cells is caused by Vif ( viral infectivity factor ) . APOBEC3G ( apolipoprotein

B mRNA-editing enzyme, catalytic polypeptidelike 3G ) is identified late, belonging to a household of enzymes called cytidine deaminases. This protein interacts with Vif. During rearward written text Cs are converted into Us after the merger of APOBEC3G in the mark cell. There are two impacts of this procedure on virus, fix enzymes of the host cel uracil DNA degrades the freshly synthesized viral DNA and secondly, hypermutation of Deoxyribonucleic acid from G toA. Expression of APOBEC3G is low in the cells leting Vif to adhere.


Viral DNA, after finalisation of contrary written text, has more molecular mass incorporating cellular and viral proteins. Preintegration composite ( PIC ) is transported to nucleus. Along with the there are certain other proteins like matrix ( MA ) , viral protein R ( Vpr ) , the in enzyme ( IN ) that are used to do a Deoxyribonucleic acid flap. Integration of viral DNA into host cell chromosome is catalysed by IN. intramolecular integrating reactions are mediated by salt stripped PIC. Refined PIC contains many cellular protein i.e. barrier to auto-integration factor ( BAF ) which is 89 aminic acids long. HMGa1 is high mobility group protein, INi-1 consisting of sections of SNFaa‚¬ ” SWI ( sucrose nonfermentingaa‚¬ ” switch ) . LEDGF/p75 lens epithelium-derived growing factor is reported to hold an interaction with IN and have engagement in integrating.

Envelop protein ( env )

HIV-1 has enveloped protein which is responsible for ordinance entry of virus into host cells. The Env cistron encodes a protein gp160. After station translational alterations, envelop is cleaved by peptidase enzyme to hold gp120 and gp41. This procedure is simple for the happening of viral infection. HIV cell surface receptors and coreceptors are bounded specifically by GP120, a surface fractional monetary unit ( SU ) protein. There is a transmembrane protein ( TM ) GP41 that has two coiling reigons HR1 and HR2 with a merger peptide. Gp120 and gp41 are attached to each other through non covalent adhering on the viral membrane. Entry of viral nucleus is initiated by first binding to the receptor, coreceptor and finally membrane merger. Conformational alterations occur in gp120 after specific binding of gp120 to CD4 cell. This alteration helps in the exposure of coreceptor adhering sites CCR5 and CXCR4. These coreceptors are recognized by V3 cringle of gp120. At this certain point, formation of merger pore begins. A six coiling package construction is formed after the 2nd conformational alteration that occurs by the interaction of HR1 and HR2 in gp41.

Transportation of viral nucleus

After entry, viral nucleus has to supply its familial stuff into the host cell nucleus. Research

showed that virus usage microtubules fot supplying its familial stuff into the karyon. Largely atthis clip, retroviruses become accessible for the host cell limitation enzymes to do mutant in them such as APOBEC3G and Trim5.

There are three spheres of uncleaved HIV-1, membrane targeting ( M ) , interaction ( I ) , tardily ( L ) domains. These three spheres play a critical function in the assembly procedure. Coevals of HIV-1 enclosed atoms is propagated by two important stairss, assembly and budding. These noxious atoms are comprised of three structural proteins nucleocapsid ( NC ) , matrix ( MA ) and mirid bug ( CA ) along with the viral Env. Nucleocapsod is responsible for interaction with viral genomic RNA. The interior covering of the viral membrane is composed of matrix while conelike mirid bug is composed of mirid bug. The viral RNA is confined within this mirid bug. Coevals of the three proteins is processed by HIV-1p55 polyprotien which is accompanied by viral peptidase ( PR ) . Besides these maps, MA, NC, CA and p55 possess a sphere p6 which is known to be necessary for the procedure of viral budding.


TSG101 is a factor that is involved in the procedure of budding. This TSG101 interacts with PTAP motive. Mutants in the PTAP motive inhibit the procedure of budding by quashing TSG101 by siRNA. In HIV-1 budding, this association is vitally of import. TSG101 is structurally similar protein to VPs23, a barm protein involved in the vacuolar sorting system. it is a fractional monetary unit of endosomal screening composites required for transport ESCRT-1 composite. Multivascular organic structures ( MVB ) generation machinery and plasma membrane are reformed by HIV-1 to advance the procedure of budding. In L sphere, there is a part that besides supports the procedure of budding. This part contain a protein AIP-1 which interacts with ESCRT-III composite. Different research groups have shown that interaction of AIP1 and TSG101 with ESCRT composite at the budding sites allow ESCRT to transport on budding and fission procedure.

Glycosylation is one of the most of import maps in the viral alteration. It has to make a batch with the construction and map, the mechanism of which is still non to the full understood. Scientists are still working at their best to detect better tools to understand the procedure of glycolysation and its importance in wellness and disease conditions. Glycolysation shows its importance in station translational alterations in for protein operation in the mammalian genome. Past research has helped us to understand that there are certain enzymes and maps involved in the biological procedures such as, signal transduction, molecular trafficking, cell adhesion, receptor activation and endocytosis. N-linked glycolysation is one of the common protein alterations. A high mannose nucleus is attached to the amide nitrogen aspargine Asn-X-Ser/Thr. This procedure, after fond regard in the early protein synthesis, is followed by a complex procedure of paring and reconstructing of oligosaccharides during when they are being transited through endoplasmic Reticulum and Golgi setup. This procedure consequences in glycolysation and holding different oligosaccharide constructions. Viruss use this cell procedure in the alteration of their surface proteins. This alteration helps the viral glycoprtiens in stableness, antigenicity and host cell invasion.

Recent surveies have provided grounds of use of glycolysation tracts by the virus including the descriptions of fond regard of N-linked oligosaccharides. This procedure causes two alterations in the viral life rhythm.

Surface proteins or N-linked glycolysation can use the host cell chaperons and turn uping factors in order to advance the proper folding and trafficking. Viruses that have been studided now show that they use calnexin and/or calreticulin for turn uping. Site of glycolysation is of import as it can impact the proper folding, endurance and transmissibility of the virus, which will act upon the proteins of the whole molecule. Other alterations in the glycolysation can do the virus to be more recognized by the host immune system, as these alterations will be holding an impact on the receptors.

HIV is one of the viruses that use glycolysation for the sweetening of their pathogenicity and immune equivocation. HIV envelop protein ( gp120 ) is composed of many mannose and glycosylated proteins. Carbohydrate on the surface of mature gp120 molecule plays a critical function in the interaction of CD4 and gp120. Earlier surveies revealed that loss of glycan affects this interaction of virus with CD4 cells but this interaction is non suppressed. As a consequence of this reduced interaction with CD4 cell, infectivity and cytopathicity will besides be decreased. Harmonizing to a globally collected information for HIV gp120 sequences, showed that there are about 25 N-linked glycolysation sites. During the class of infection, V1-V2 envelop cringle has sequences for the add-on of glycosylation due to which change occurs in sensitiveness and neutralizing antibody. N-linked glycans within these V1-V2 cringle holding 15 discrepancies is needed to advance viral infection and cut down its sensitiveness to serum antibody. However, the inquiry arises how the part of N-linked glycolysation provides protection as many glycans are preserved in gp120. We have an illustration of human monoclonal antibody 2G12 that acts on the antigenic determinant of gp120 holding high mannose and/or intercrossed glycans. The antigenic determinant was composed of mannose dependent saccharide and was found as a extremely preserved reigon of gp120. After analysing it was observed that D1 and D3 weaponries of Man9GlcNAc2 are really of import, in the interaction with 2G12 neutralizing antibody. The antigenic determinant of gp120 plays a critical function in doing infection as it is thought to believe that mannaose dependent fond regard of HIV with mannose receptor ( MMR ) , promotes the entry into the host cells. Mutants and successional add-ons in the N-glycan sites provide a protective glycan shield which protects the virus against host neutralizing antibodies. By this it is being concluded that glycolysation is non entirely, but partially responsible in bring forthing the opposition against host neutralizing antibodies.



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