An Analysis on Primary HIV Disease: A Case Study of Innate Defense Activation and Reactions System

The invulnerable framework contains complex cell and humoral frameworks, which are structuring an intelligent system to distinguish and destroy attacking pathogens. Outside particles exhibit on infections, microscopic organisms and parasites, however not on host units, are segregated from self through pathogen-copartnered sub-atomic examples. Upon passage of the pathogen into the figure prompt non-particular resistant reactions are triggered and inside a short time the innate invulnerable framework is totally enacted. The innate safe framework is made out of different humoral and cell players, incorporating cytokines, supplement proteins, intense stage proteins, dendritic cells, macrophages, NK cells, that co-work in a perplexing to produce an powerful protection against contamination. Even from an optimistic standpoint, the aforementioned prompt innate resistant reactions have the ability to clear contamination or span the period until the adjustable, particular insusceptible reaction is producing results.

Among the first components activated during the innate immune response is the complement system that together with interferons, cytokines and chemokines stimulate innate immune cells, such as dendritic cells (DCs), natural killer (NK) cells, natural killer T (NKT) cells, monocytes, or macrophages. These factors act in concert until the adaptive arm of immunity is established. Thus, to control the infection process in the acute phase a coordinated action of the innate immune elements is essential. In the beginning of an infection viruses and microbes developed different strategies to avoid he attack of the innate immune system. Also the human immunodeficiency virus (HIV) is able to overcome innate and adaptive immune responses in

Viral contaminations bring about an in number actuation of the innate invulnerable framework that is emulated by the advancement of adjustable resistant reactions. Examines in distinctive models of viral contaminations, and in addition investigations of inoculation, have further exhibited that the value of the beginning innate insusceptible reaction is nearly connected to, and in certain studies predicts, the capacity of the consequent versatile insusceptible reactions to pathogens. This cross-talk between innate and adjustable resistance is misused in vaccines by utilizing adjuvants invigorating particular innate invulnerable pathways. Spoiling with human immunodeficiency infection sort 1 (HIV-1) does not vary from other viral contaminations in initiating the insusceptible framework, and a few studies have now exhibited noteworthy actuation of segments of the innate invulnerable framework in essential HIV-1 tainting, going before the infrastructure of adjustable B and T cell reactions. Almost no is grasped, on the other hand, about the part of innate invulnerability in HIV-1 pathogenesis and the results of the cross-talk between innate and versatile insusceptible reactions in essential contamination for invulnerable control of HIV-1 tainting. In this survey, we will highlight a portion of the information exhibited at a later symposium on intense HIV-1 tainting in Boston, and in addition circulated information on innate insusceptibility in essential HIV-1 tainting. Unique center is given to the part of sort I Ifns and characteristic executioner (NK) cells in HIV-1 sickness, 2 regions of research that appropriated respectable consideration throughout the symposium. Myeloid cells, incorporating dendritic units and macrophages, play a vital part in the innate and adjustable resistant reaction against viral pathogens like HIV. Myeloid cells are likewise critical focuses of HIV and SIV. Macrophages and dendritic cells (Dcs) express the indispensible receptors (Cd4 and chemokine co-receptor(s)) needed for HIV-1 entrance and, for instance Cd4+ T cells, are near the most punctual focuses for HIV-1 and SIV in vivo , (looked into in ). HIV and SIV have been recognized in macrophages in auxiliary lymphoid tissue by in situ hybridization in vivo . Also, at later phases of pathogenesis, HIV spoiled macrophages are thought to be the explanation for Aids identified encephalopathy , and SIV contaminated macrophages make a practically equivalent to mid apprehenSIVe framework pathology in the rhesus macaque model . In any case, myeloid cells are to some degree impervious to HIV and SIV spoiling since they express abnormal amounts of host confinement calculates that stand for noteworthy post-section squares to HIV-1 contamination. viral particles by C-sort lectin receptors, a family that incorporates Dc-particular intercellular bond atom 3-getting nonintegrin (Dc-Sign), and mannose tying C-sort lectin receptors (Mclr) . A heparin sulfate proteoglycan subordinate pathway and a cholesterol-ward pathway for disguise of whole viral particles have additionally been portrayed. All the more not long ago, it was demonstrated that sialyllactose is an atomic distinguishment design in gangliosides in the HIV-1 film that permits Dcs to catch viral particles. What's more, galactosyl ceramide can intervene unit to cell exchange of HIV-1 from dendritic cells to T lymphocytes. Beneficial spoiling of Dcs with HIV-1 has additionally been accounted for in vitro. Notwithstanding, just a minor rate of Dcs have been discovered to be tainted in vivo and most confirmation shows that Dcs don't reproduce HIV prudently. Consequently, the commitment of HIV tainting of Dcs to pathogenesis needs further study. It is conceivable that the essential part of Dcs in HIV illness is to transmit disguised viral particles to Cd4+ T units instead of to straightforwardly underpin profitable tainting (surveyed in). Non-self recognition of an invading microbial pathogen is a first and critical step in programming the host immune system for control of infection. Mammalian cells recognize microbial invaders through the actions of a wide variety of pathogen recognition receptor (PRR) molecules. PRRs serve to distinguish self from non‑self by virtue of their recognition of and interaction with pathogen‑specific macromolecules, termed pathogen associated molecular patterns (PAMPs). Human cells variably express a variety of PRRs, including the RIG-I like receptors (RLRs), Toll-like receptors (TLRs), NOD-like receptors (NLRs), as well as other less defined sensors (such as those responsible for sensing cytoplasmic DNA, specific carbohydrates, and certain lipids).1‑4 Differential compartmentalization of PRRs, as well as their cell‑specific expression, creates a comprehenSIVe and complex network for PAMP sensing dedicated to immune signaling. PAMPs encompass a wide range of moieties, including protein, nucleic acids, lipids, and certain carbohydrates or combinations of each, that harbor structural signatures of a particular pathogen or group of pathogens. These molecules differ from host cell macromolecules sufficiently in structure, location, and/or interactions such that they are discriminated as non‑self through PRR interaction. Non‑self recognition and PAMP binding by PRRs leads to the rapid engagement of downstream intracellular signaling cascades that activate a variety of host transcription factors. This process lead to alteration of host cell gene expression and induction of intracellular immune defenses termed the innate immune response. In terms of virus infection, this response drives the expression of a variety of genes directly induced by PRR signaling and indirectly induced by secreted product from the

encode a variety of antiviral products, proinflammatory cytokines and chemokines that that respectively function to directly limit virus replication and to induce antiviral innate immune responses while attracting and modulating adaptive immune cells to the site of infection. Type 1 interferon (IFN) is a major product of PRR signaling and is produced and secreted from the infected cell. IFN binds to its receptor in autocrine and paracrine fashion to drive the expression of hundreds of interferon stimulated genes (ISGs) within the infected cell and in the surrounding tissue. ISG products mediate antiviral, immunomodulatory, metabolic, and proapoptotic actions that suppress virus infection and stimulate the adaptive immune response 2,5 to mediate a systemic antiviral state.

HIV is a retrovirus, from the family lentiviridae. It is quite nearly identified with simian immunodeficiency infections (SIV) which particularly contaminates types of old planet moNKeys. The infection comprises of an encompassed capsid structure holding a mixed bag of viral and have proteins, and two Rna duplicates of the viral genome. In the wake of captivating its related receptors and co-receptors on target cells, the viral envelope proteins experience structural updates accelerating combination of the viral envelope with the layer of the target unit, bringing about discharge of the viral center and its substance into the host. The HIV Rna genome experiences reverse interpretation soon after discharge into the cell, accelerating the processing of a Proviral Dna duplicate which then translocates over the atomic layer into the core where the now double-stranded hereditary material is embedded into the host genome. This embedded Dna then comes to be the template for generation of viral Rna from the viral Long‑terminal Repeat (Ltr) promoter, creating Rna atoms to be made as viral proteins, and the wellspring of full length genomic Rna species which will possibly be bundled into new offspring infection. Interpretation of HIV proviral Dna gives ascent to various diverse Rna transcripts of different lengths, which prompt the generation of nine diverse gene features. The aforementioned proteins explain the structural and enzymatic lands of the infection, and also numerous embellishment gene features which are answerable for balancing the host environment to profit the infection and push replication and viral development. HIV has an exceptionally different cell tropism, resolved by the representation of the HIV receptor Cd4, and also the articulation of co-receptors, fundamentally Ccr5 and Cxcr4. Representation of the aforementioned particles is selective to particular myeloid unit and lymphocyte subsets, which guides HIV tainting to the major insusceptible cell compartment, to annihilating impact. Spread of the blood stream and from individual to individual through organic liquid contact, above all commonly through sexual contact and intravenous drug utilization. This puts the infection in contact with various target units of infection. Spoiling with HIV is described by an introductory intense stage of contamination, throughout which time the infection recreates extremely abnormal amounts, basically contaminating Cd4+ lymphocytes. This stage of malady is likewise described by an increment in turnover of Cd4+ lymphocytes. Therefore, the phase of crest viral spoiling holds waves of recently integrated HIV contaminating natural Cd4+ lymphocytes, which then produce more infection, and are quickly murdered or cleared. In the long run HIV-specific insusceptible reactions are incited and start to control the level of viremia. The aforementioned reactions comprise of both cytotoxic Cd8+ T-lymphocyte (Ctl) and Cd4+ T-helper-mediated humoral reactions. Adjustable insusceptible reactions are finally deficient to control contamination, and patients will regularly advancement to Supports, described by Cd4+ T-cell exhaustion and corruption of the insusceptible compartment expediting immunodeficiency and shrewd contaminations.

Notwithstanding the enactment of PDCS through innate design distinguishment receptors, intense HIV-1 tainting additionally brings about the enactment and extension of NK cells. To some degree, this enactment of NK cells may be brought about by the elevated amounts of proinflammatory cytokines discharged by Dcs and monocytes, incorporating Il-15 and IFN-a. Starting studies showed a huge development of NK cell numbers in intense HIV-1 tainting, specifically soon after the improvement of any distinguishable counter acting agent reactions. After this starting extension of exceptionally actuated NK cells, NK cells come to be progresSIVely disabled, with enduring viral replication and sickness movement. This disability of NK cell capacity with continuous HIV-1 illness is co-partnered with a collection of Cd56low NK cells that are anergic to stimulation. NK cells constitute a quite heterogenic cell populace in a given single, comprising of various distinctive NK cell clones described by differential receptor declaration profiles, incorporating diverse actuating and inhibitory executioner unit immunoglobulin- like receptors (KIRS). The fusion of actuating and inhibitory KIRS, in conjunction with their HLA class I ligands, verifies the purpose of NK units and their capacity to react to virally spoiled target units. Later studies have demonstrated that particular consolidations of KIR genotypes, in

slower HIV-1 ailment movement. Specifically, the interpretation of the initiating receptor Kir3ds1 in conjunction with its putative HLA class I ligands, HLA class I particles of the Hla-Bw4–80i family (counting HLA class I alleles, for example Hla-B57 and Hla-B51) has been connected with slower ailment movement . Likewise, the vicinity of subtypes of the inhibitory receptor Kir3dl1 connected with higher declaration levels of Kir3dl1 on NK units has been demonstrated to fine-adjust the defenSIVe impact of HLA class I alleles of the Hla-Bw4–80i family. Besides, a specific nucleotide polymorphism connected with higher declaration levels of HLA-C, the central ligand for receptors of the Kir2dl and Kir2ds family, has been demonstrated to be connected with more level viral set indicate and slower malady movement . Findings of these epidemiological studies strongly suggest that specific subsets of NK cells from individuals expressing particular receptor or ligand genotypes can mediate better control of HIV-1 replication. Functional studies demonstrating that KIR3DS1+ NK cells can strongly inhibit HIV-1 replication in CD4+ T cells expressing HLA-Bw4–80I in vitro provide further support for this model. Interestingly, the KIR/HLA class I compound genotypes also appear to modulate the ability of specific NK cell subsets to expand preferentially during acute HIV-1 infection. Recent data show that KIR3DS1+ NK cells, and to a lesser extent KIR3DL1+ NK cells, are over proportionally expanded in primary HIV-1 infection, but only in individuals who also encode for HLA class I molecules of the HLABw4–80I family, not individuals negative for HLA-Bw4–80I. Further studies need to investigate whether the preferential expansion of these NK cells expressing KIRs associated with better HIV-1 disease outcome represent a functional correlate of protective immunity. However, apart from their role in eliminating HIV-1–infected cells, NK cells might also be involved in killing uninfected CD4+ T cells expressing ligands for activating NK cell receptors, as a consequence of bystander activation, thereby contributing to CD4+ T cell decline. Apart from their direct antiviral activity, NK cells play an important role in modulating DC function. NK cells are involved in the rapid elimination of immature DCs, which aberrantly enter the peripheral circulation, while sparing mature DCs, owing to differences in major histocompatibility complex class I expression. This NK cell–mediated quality control of DC populations ensures that only immunogenic mature DCs are able to gain access to inductive sites. Recent studies have demonstrated that the ability of NK cells to eliminate immature DCs is severely impaired in chronic HIV-1 infection, and this impairment of the quality control function of NK cells might have a significant effect on the ability of DCs to induce antiviral T cell responses. These data suggest that NK cells play an important

Almost no is known regarding the most punctual occasions after HIV transmission in the genital tract on the other hand the rectal mucosa and above all discoveries about the aforementioned early occasions were procured from in vivo models of SIV-tainted macaques (Haase, 2005). The in vivo SIV models and ex vivo dissections in the human framework follow to recognize cells and solvent calculates included in HIVtransmission (Haase, 2005; Hladik and Mcelrath, 2008). R5-tropic HIV-1 particles are specifically caught by epithelial cells and consequently transferred to Ccr5-communicating target cells underneath the epithelia. This could be answerable for the specific special transmission of R5-tropic HIV-1 strains (Meng et al., 2002). Langerhans cells (LCS) or other dendritic cells are available at the port of the mucosal passage site (in the underlying tissues of the vagina and cervix) and trap pathogens with their methods that stretch out to the luminal surface. Consequently, infections cross the mucosal obstruction by connection or tainting of DCS, by transcytosis (M cells) or by tainting of intraepithelial lymphocytes and macrophages. Different cells of the innate resistant framework explain constructing the first line barrier against HIV until the versatile resistant reaction is completely advanced. Dendritic cells in intense HIV tainting: Dendritic cells are the most strong antigen-displaying cells and might be isolated into traditional myeloid Dcs (Lcs, dermal Dcs, blood Dcs) and plasmacytoid DCS (Table 1, adjusts from Altfeld et al., 2011). They vary regarding their area, their C-sort lectin and Tlr articulation, their part in HIV-tainting, their cytokine processing and their capacity. Langerhans cells and HIV: Langerhans cells (LCS) construct the first line resistance against mucosal contaminations in light of the fact that they are arranged conceivably in mucosal tissues to get pathogens. LCS overview the basal and suprabasal layers of the stratified squamous epithelium of the skin and oral and ano-genital mucosa for attacking pathogens (Katz et al., 1979; Romani et al., 1985; rev. in Dejong and Geijtenbeek, 2010). Upon catch of Ags, LCS begin to develop, which is stood for by upregulation of Ccr7, co-stimulatory atoms Cd80/cd86/cd40, MHC class I and class Ii atoms and Cd83 and by down-regulation of Langerin and E-cadherin (Merad et al., 2008). The aforementioned adult Lcs relocate to the lymph junction to exhibit the caught Ag to T cells, in this manner inciting a productive resistant reaction (Merad et al., 2008). Dermal dendritic cells and HIV : notwithstanding Lcs, interstitial dendritic units are near the first units to

underlying the epithelium and vary from Lcs, since they don't hold Birbeck granules and express heterogenous measures of Cd1a (Bell et al., 1999). Interstitial Dcs are limited in the dermis and oral, vaginal and colonic lamina propria (Pavli et al., 1990, 1993; Lenz et al., 1993; Nestle et al., 1993; Mclellan et al., 1998). HIV-spoiled people may have a down-regulation in intracellular perforin and granzyme A stores, which might elucidate the diminished cytotoxic limit of NK cells in HIV-spoiling (Portales et al., 2003). Macrophages in intense HIV spoiling: Macrophages inhabitant at mucosal destinations are proposed to play a critical part throughout HIV-1 pathogenesis. Macrophages span innate and versatile invulnerability comparable to DCS, NK and NK T units. They are distinguishing; disguising and debasing microorganisms and clear unit trash through TLRS, C-sort lectins (Dectin-1), Fc receptors and supplement receptor 3. Besides, macrophages present pathogen-inferred peptides through Mhc class Ii, accordingly starting versatile invulnerable reactions, and mystery expert incendiary cytokines. Upon HIV-spoiling they are right around the first cells experienced by the infection, yet they are fit to oppose to HIV-intervened cytopathic impacts. Consequently, macrophages are thought to serve as major cell HIV supply together with inactively spoiled resting Cd4+ T cells for lifelong spoiling. Profitably tainted macrophages were identified in both untreated patients and those appropriating antiretroviral help (Art), however the HIV contamination inside macrophages was not connected with infection actuated cytopathic impacts (Koenig et al, 1986; Sharkey et al, 2000). The irresistible infection is held in macrophages for a delayed time of time and the infection may be discharged from macrophages postponed and in a diverse compartment – in this way macrophages donate to ingenuity and spread of the infection (Crowe et al., 2003; Montaner et al., 2006; Carter and Ehrlich, 2008). As located in NK or NK T units, the capacities of macrophages were discovered to be disabled by HIV-1 contamination in vitro and in vivo. In vivo macrophages from HIV-tainted people were discovered to be inadequate for phagocytosis of apopotic cells (Torre et al., 2002). In vitro HIV-1 blocked with phagocytosis through Cr3 or Fcr and likewise hindered disguise of Candida albicans and Toxoplasma gondii (Crowe et al., 1994; Kedzierska et al., 2002; Azzam et al., 2006; Leeansyah et al., 2007). As not long ago indicated, Nef was an essential element in upsetting phagocytosis in HIV-1–infected units (Mazzolini et al., 2010). Monocytes in intense HIV contamination: Similar to Dcs, LCS and macrophages, monocytes give a first in as crux middle people of innate insusceptible instruments. On the other hand, they are likewise focuses for monocyte-tropic pathogens, for example Listeria, cytomegalovirus and HIV (Drevets and Leenen, 2000). Monocytes express Cd4, Ccr5 and Cxcr4 and are in specific vulnerable to macrophage-tropic HIV strains. Comparable to macrophages, monocytes are impervious to the cytopathic impacts of HIV, they stand for a nexus infection repository and might likewise disperse HIV in distinctive areas for example the mind (Kedzierska and Crowe, 2002; Crow et al., 2003). Promptly in intense spoiling, HIV and SIV drop in the midway apprehenSIVe framework (CNS) and macrophages and monocytes appear to play a urgent part in the neuropath genesis of HIV-contamination and to donate to HIV-intervened dementia because of handling of genius incendiary cytokines and neurotoxins (Chakrabarti et al., 1991; Kedzierska and Crowe, 2002). The impelling of genius incendiary cytokines is thought to expedite the section of monocytes into the mind by upsetting the blood-mind and blood cerebrospinal liquid boundary (Persidsky et al., 2000; Eugenin and Berman, 2003).

Recent studies have uncovered a variety of evidence to indicate that innate immune activation may actually have pathogenic consequences for HIV infection, and that HIV-1 may actually benefit from our immune system attempting to control and clear infection. First, activation of innate defenses and the stimulation of inflammation drives the infiltration of many more target cells into the infection site, thus supporting HIV expansion into these incoming CD4+ cells. This paradox is at the heart of HIV infection. Additionally, there is powerful evidence that the initial systemic breakout of the virus during acute infection is accompanied by very high levels of IFN, cytokines, and chemokines. This “cytokine storm” is present without imparting control of the virus via traditional cell‑mediated innate mechanisms. Of note is that TLR agonists have also been applied to macaques in an SIV infection model in which these compounds were expected to drive innate immune activation and suppression of the infection but instead they actually resulted in a major increase in the efficiency and spread of the acute infection. Finally, several studies comparing “pathogenic” and non-pathogenic SIV infections in non-human primate models have demonstrated a protracted, less controlled innate immune response in the pathogenic infections, suggesting that too much innate immune activation is at least partially responsible for pathogenesis of infection. Importantly, there is a substantial amount of evidence that innate immune signaling can control HIV infection, and that the virus is actively modulating the host environment to control these defenses. IFN can inhibit HIV growth, and there are many ISGs with known

been shown to be under strong evolutionary pressure, again supporting the importance of these factors, and work has shown that HIV has evolved specific mechanisms for antagonizing the cell intrinsic innate signaling pathways to avoid the anti‑viral state.76 So what should be taken away from these seemingly contradictory observations of innate immunity regulation, immune activation, and pathogenesis of HIV infection? First, all innate immune responses are not created equal, and that the appropriate activity to protect the host from infection is most likely highly context dependent. Work with various vaccine and agonist systems have elegantly shown that very different immune responses can be driven by different stimuli, and that the most appropriate response is dependent on the pathogen.100,101 For example, TLR7/9 agonists are inappropriate as antivirals or vaccine adjuvants unless it is shown that they impart the innate immune response similar to that naturally induced by non-pathogenic lent viruses or by HIV variants that have lost ability to antagonize innate immune defenses. We currently do not understand what constitutes a successful innate immune response against HIV and what immune parameters successfully mediate protection from future HIV challenge. Obviously, more research is needed to inform agonist and vaccine design strategies but it is likely that innate immune stimulation and regulation strategies will be at the heart of any immune therapy design. We also have little insight into the viral host interactions that govern immunity during the HIV during the eclipse phase, a potentially vital time for overcoming infection. Studies aimed at defining HIV replication stage‑specific innate immune programming may reveal new insights of immune regulation over the entire course of infection. Second, the data from in vivo infection studies must be viewed in the light of innate immune dysregulation, quite possibly due to direct viral antagonism of early innate immune defense pathways. The dysregulation of the immune system which is the hallmark of HIV infection can be compared with several other model systems where innate antagonism/perturbations cause dramatic immune dysfunction. A significant amount of work with high quality mouse models of RNA virus infection have shown for instance that changes in innate signaling early in infection not only cause higher viral titers during infection, but cause major defects in downstream adaptive immune responses.61,110‑114 In fact, that removal of just the cell intrinsic signaling component of the innate immune defenses elicits major innate and adaptive immune defects, both at the cell and whole animal level and involves a dysregulation of production of proinflammatory cytokines, altered antibody profiles, altered T regulatory cell function, and increased inflammation analogous to the HIV cytokine storm and systemic immune activation.61 Thus, virus and host governance of the innate immune response must be considered in

As with other viral infections, HIV-1 infection results in an initial activation of innate immunity, followed by the development of adaptive immune responses. Innate immune responses to HIV-1 can contribute directly to the control of HIV-1 replication, might play an important role in modulating the function of the subsequent HIV-1–specific adaptive immune response, and can contribute to HIV-1 disease progression. Our understanding of the direct antiviral activity of innate immunity, and its adjuvant effect on adaptive immunity, is still very limited and needs to be expanded, to enable strategic interventions aimed at enhancing immune control of HIV-1 by modulating innate immunity while avoiding immunopathogenesis resulting from its over activation. Rather than wrecking the infection at the beginning stages of spoiling, macrophages and monocytes appear to fill in as 'trojan horse' by actively donating to the spread of HIV over long time periods. Next to Lcs and PDCS, t cells, principally found in the gastrointestinal mucosa, NK and NK T cells, that are initiated by IFN-emitted PDCS, manufacture a vital in the first place line of safeguard against viral, bacterial, and contagious pathogens. HIV-1 neutralizes this innate invulnerable hindrance by modifying their capacities and diminishing their numbers by yet essentially unclear instruments. The HIV-intervened misfortune in amounts of vital innate invulnerable cells, for example PDCS, NK and NK T cells or t units, is connected with an adjusted cytokine microenvironment, which might also explain the incessant station of HIV-tainting in the host. On the grounds that it is troublesome recognizing contaminated people extremely soon after introduction, small is known regarding the soonest occasions of HIV transmission in the genital tract or rectal mucosa. The greater part of the discoveries are determining from in vivo models of SIV tainting (rev. in Haase, 2005) and from ex vivo demonstrates meant to distinguish units and components influencing the transmission of HIV (rev. in Hladik and Mcelrath, 2008). Indeed, while utilizing animal models the precise process how the infection invades mucosal obstructions to create a beneficial contamination in the host is greatly mind boggling to assess. There are different innate dissolvable and cell elements acting together upon entrance of HIV into the host – yet, the innate systems and even the particular versatile insusceptible reactions cannot confine the replication of HIV in for the most part contaminated people demonstrating the determination of viral mutants that have the capacity to effectively escape the aforementioned early and late cell and humoral safe reactions. In the final a long time, expanding proof infers that particularly immunologic and virologic occasions occurring throughout essential tainting irreversibly debilitate the safe framework, which is

oppose viral and entrepreneurial contaminations.

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Assistant Professor, Pratap College, Amalner, Distt. Jalgaon