Brief Report - (2023) Volume 14, Issue 4
Received: 03-Aug-2023, Manuscript No. jar-23-114962;
Editor assigned: 05-Aug-2023, Pre QC No. P-114962;
Reviewed: 17-Aug-2023, QC No. Q-114962;
Revised: 22-Aug-2023, Manuscript No. R-114962;
Published:
29-Aug-2023
, DOI: 10.37421/2155-6113.2023.14.954
Citation: Kooipt, Ruesrt. “The Response to Vaccinations in People with HIV is Complicated by the Presence of the Cytomegalovirus.” J AIDS Clin Res 14 (2023): 954.
Copyright: © 2023 Kooipt R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Human Immunodeficiency Virus (HIV) remains a global health challenge, affecting millions of people worldwide. The advent of Highly Active Antiretroviral Therapy (HAART) has transformed HIV infection from a life-threatening disease to a manageable chronic condition, significantly improving the life expectancy and quality of life for individuals living with HIV. Vaccinations play a critical role in safeguarding the health of this vulnerable population, helping to prevent potentially life-threatening infections. However, the response to vaccinations in people with HIV is often complicated, and one factor that adds complexity to this issue is the presence of Cytomegalovirus (CMV). This article explores the intricate relationship between CMV and vaccination responses in individuals with HIV, shedding light on the challenges and potential strategies to optimize vaccine efficacy [1,2].
Diabetes and cardiovascular ischaemic events are significant health concerns in PLWH. The prevalence of these conditions is higher in this population compared to the general population, and they contribute significantly to morbidity and mortality. This section introduces the topic and highlights the need for understanding the role of ageing biomarkers and monocyte activation in the development of these comorbidities [3]. HIV infection has been associated with an accelerated ageing process, characterized by increased immune activation, inflammation, and cellular senescence. This section explores the mechanisms underlying accelerated ageing in PLWH and its implications for the development of diabetes and cardiovascular ischaemic events. Chronic inflammation, driven by ageing biomarkers and monocyte activation, contributes to insulin resistance, a key mechanism underlying diabetes development in PLWH. This section discusses the link between chronic inflammation, insulin resistance, and diabetes.
Ageing biomarkers, such as telomere length, epigenetic changes, and markers of cellular senescence, provide insights into the biological ageing process. This section discusses the role of ageing biomarkers in PLWH and their association with diabetes and cardiovascular ischaemic events [4,5]. Chronic immune activation and inflammation are hallmarks of HIV infection. Monocyte activation, specifically, plays a crucial role in the pathogenesis of HIVrelated comorbidities. This section examines the role of monocyte activation and the associated inflammatory response in diabetes and cardiovascular ischaemic events. Different subsets of monocytes exhibit distinct phenotypes and functional characteristics. This section explores the role of monocyte subsets in the development of diabetes and cardiovascular ischaemic events in PLWH and their potential as biomarkers for risk stratification [6].
Diabetes and cardiovascular ischaemic events pose significant challenges in the management of PLWH. The interplay between HIV infection, ageing biomarkers, and monocyte activation contributes to the development of these comorbidities. Understanding the underlying mechanisms and identifying biomarkers can aid in risk stratification, early detection, and targeted interventions. By addressing these factors, healthcare providers can improve the management and prevention of diabetes and cardiovascular ischaemic events in PLWH, ultimately enhancing their overall health outcomes.
None.
None.
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Journal of AIDS & Clinical Research received 5061 citations as per Google Scholar report