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HIV in Iran: onset, responses, and future directions.

ABSTRACT: Iran, a country in the Middle East and North Africa (MENA) region, has been actively involved in the fight against HIV/AIDS over the past three decades. The unique features of the HIV epidemic in Iran are reflected by the modes of transmission and its recent changes to improve management and prevention programs. In this review, we recount the initial onset and subsequent spread of HIV infection in Iran, beginning with the first case diagnosed to the ongoing responses and most recent achievements in controlling this epidemic. Although in the MENA region, Iran is one of the pioneers in implementing pertinent policies including harm reduction services to decrease HIV incidence, drug injection still continues to be the major risk of infection. In line with other nations, the programs in Iran aim at the UNAIDS 90-90-90 targets (UNAIDS 90-90-90 global targets to end the AIDS epidemic by 2020: by 2020, 90% of all people living with HIV will know their HIV status; 90% of all people with diagnosed HIV infection will receive sustained antiretroviral therapy; and 90% of all people receiving antiretroviral therapy will have viral suppression) and to eliminate mother-to-child HIV transmission. In this article, we discuss the strengths and shortcomings of the current HIV programs and offer suggestions to provide a better perspective to track and respond to the HIV epidemic. More generally, our account of the national religious and cultural circumstances as well as obstacles to the approaches chosen can provide insights for decision-makers in other countries and institutions with comparable settings and infrastructures.

SUBMITTER: SeyedAlinaghi S

PROVIDER: S-EPMC7924262 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Glucocorticoids are the most effective anti-inflammatory therapy for asthma yet are relatively ineffective in chronic obstructive pulmonary disease. Glucocorticoids suppress inflammation via several molecular mechanisms. Glucocorticoids suppress the multiple inflammatory genes that are activated in chronic inflammatory diseases, such as asthma, by reversing histone acetylation of activated inflammatory genes through binding of ligand-bound glucocorticoid receptors (GR) to co-activator molecules and recruitment of histone deacetylase-2 to the activated inflammatory gene transcription complex (trans-repression). At higher concentrations of glucocorticoids GR homodimers interact with DNA recognition sites to activate transcription through increased histone acetylation of anti-inflammatory genes and transcription of several genes linked to glucocorticoid side effects (trans-activation). Glucocorticoids also have post-transcriptional effects and decrease stability of some pro-inflammatory mRNA species. Decreased glucocorticoid responsiveness is found in patients with severe asthma and asthmatics who smoke, as well as in all patients with chronic obstructive pulmonary disease. Several molecular mechanisms of glucocorticoid resistance have now been identified which involve post-translational modifications of GR. Histone deacetylase-2 is markedly reduced in activity and expression as a result of oxidative/nitrative stress so that inflammation becomes resistant to the anti-inflammatory actions of glucocorticoids. Dissociated glucocorticoids and selective GR modulators which show improved trans-repression over trans-activation effects have been developed to reduce side effects, but so far it has been difficult to dissociate anti-inflammatory effects from adverse effects. In patients with glucocorticoid resistance alternative anti-inflammatory treatments are being investigated as well as drugs that may reverse the molecular mechanisms of glucocorticoid resistance.

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HIV in Iran: onset, responses, and future directions.

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