डिमेंशिया का जर्नल

खुला एक्सेस

हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।

ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं

अमूर्त

Genetic Variations of V3 and C3 regions in gp120 protein of HIV-1 env gene

Hari Om Singh, Vivek Gupta and Amita Singh

Background: HIV-associated neurocognitive disorder (HAND) is an important cause of morbidity of HIV patients. The development of neurological disease among individuals having an HIV infection is variable. The env sequences of HIV-1 are important for cell entry and neurotropism. The env sequences vary among individuals having HIV infection. Hence the development of neurotoxicity differs among individuals with HIV infection. So far, none of the studies reported the mechanism of neurotoxicity in astrocytes. Hence we comprehended the genetic profile of the gp120 protein of HIV-1 env gene which influences the pathogenesis of neurocognitive diseases

Method: We led the search utilizing multiple databases, specifically, EMBASE, PubMed (Medline), and Google Scholar.

Description: Pathogenesis of HAND is influenced by HIV-1 env sequences. The gp120 glycoprotein serves as a determinant to cross the blood-brain barrier and maintain neurocognitive impairments. The persistence of env sequences within the CNS leads to neurovirulent features and neurotoxicity. The evolution of the env gene is a continuing process that contributes to neurocognitive disease severity.

Conclusion: Genetic profiling of V3 and C3 regions of gp120 motifs in a larger number of HAND patients with various ethnic groups will provide data for the correlation of V3 and C3 regions with IHDS and cognition parameters. This will help to define the risk factor which can contribute to neurocognitive disease.