Search Results (7)

HIV/AIDS remains a global public health concern, with a high prevalence in sub-Saharan Africa. The President’s Emergency Plan for AIDS Relief (PEPFAR) initiatives, including preexposure prophylaxis (PREP) and postexposure prophylaxis (PEP), significantly reduced HIV infections in South Africa and Nigeria. The suspension of United States (U.S.) foreign aid may impact these preventive measures. Although some emergency aid programs were exempted, uncertainty persists, impacting global health initiatives, especially in South Africa and Nigeria. This study investigates the public health impacts of the United States (U.S.) government’s January 2025 suspension of U.S. foreign aid, focusing on its implications for HIV prevention initiatives, such as PREP and PEP, in South Africa and Nigeria. We comprehensively searched keywords such as PEPFAR, PREP, PEP, HIV infection in South Africa or Nigeria, antiretroviral (ARV) drugs, public healthcare impact, 2025 Trump’s foreign aid withdrawal, titles, and abstracts in Google Scholar, PubMed, and Web of Science. The search results were screened from 500 to 150 included articles based on their relevance and quality assessment for inclusion. The review unveiled that Nigeria maintained a continuous increase in HIV/AIDS-related deaths and new HIV infections from 1990, reaching the climax between 1999 and 2005, showing approximately 110,000 HIV/AIDS-related deaths and 200,000 new HIV infections. Notably, due to the PEPFAR intervention in Nigeria, an improved decrease in both HIV/AIDS-related deaths (45,000) and new HIV infections (75,000) was experienced from 2010 to 2023. South Africa experienced a rapid increase between 1990 and 2003 in both HIV/AIDS-related deaths and new HIV infections, reaching the climax around the early 2000s, with about 520,000 new HIV infections and 260,000 HIV/AIDS-related deaths in 2005. Furthermore, there was a continuous decline from 2005 onwards, with 50,000 HIV/AIDS-related deaths and 150,000 new HIV infections by 2023. Therefore, the suspension of this aid threatens disruptions in ARV therapy, possible increases in HIV transmission, shortages in PREP and PEP, the retrenchment of healthcare workers, the suspension of non-governmental organization activities, and the reversal of gains in vulnerable populations, reversing progress toward the 95-95-95 vision, increasing morbidity and mortality rates and financial strain on healthcare systems in these two countries. We recommend proactive measures, such as increased budget allocations for healthcare reforms, exploring local vaccine and health product development and diversifying funding sources in Nigeria, and implementing universal healthcare coverage for South Africans to mitigate the adverse consequences of aid withdrawal. Full article

Human immunodeficiency virus (HIV) and hepatitis B virus (HBV) continue to be global public health issues. Globally, about 39.9 million persons live with HIV in 2023, according to the Joint United Nations Programme on HIV/AIDS (UNAIDS) 2024 Fact Sheet. Consequently, the World Health Organisation (WHO) reported that about 1.5 million new cases of HBV occur, with approximately 820 thousand mortalities yearly. Conversely, the lower percentage of HBV (30%) cases that receive a diagnosis is a setback in achieving the WHO 2030 target for zero HBV globally. This has necessitated a public health concern to repurpose antiretroviral (ARV) drugs for the treatment of HBV diseases. This review provides an introductory background, including the pros and cons of repurposing antiretrovirals (ARVs) for HBV treatment. We examine the similarities in replication mechanisms between HIV and HBV. We further investigate some clinical studies and trials of co-infected and mono-infected patients with HIV–HBV. The topical keywords including repurposing ARV drugs, repurposing antiretroviral therapy, Hepatitis B drugs, HBV therapy, title, and abstracts are searched in PubMed, Web of Science, and Google Scholar. The advanced search includes the search period 2014–2024, full text, clinical trials, randomized control trials, and review. The search results filtered from 361 to 51 relevant articles. The investigations revealed that HIV and HBV replicate via a common route known as ‘reverse transcription’. Clinical trial results indicate that an early initiation of ARVs, particularly with tenofovir disoproxil fumarate (TDF) as part of a regimen, significantly reduced the HBV viral load in co-infected patients. In mono-infected HBV, timely and correct precise medication is essential for HBV viral load reduction. Therefore, genetic profiling is pivotal for successful ARV drug repurposing in HBV treatment. Pharmacogenetics enables the prediction of the right dosages, specific individual responses, and reactions. This study uniquely explores the intersection of pharmacogenetics and drug repurposing for optimized HBV therapy. Additional in vivo, clinical trials, and in silico research are important for validation of the potency, optimum dosage, and safety of repurposed antiretrovirals in HBV therapy. Furthermore, a prioritization of research collaborations comprising of regulators and funders to foster clinically adopting and incorporating repurposed ARVs for HBV therapy is recommended. Full article

Background/Objectives: This review aims to provide a comprehensive understanding of how HIV alters normal aging trajectories in the brain, presenting the HIV-related molecular mechanisms and pathophysiological pathways involved in brain aging. The review explores the roles of inflammation, oxidative stress, and viral persistence in the brain, highlighting how these factors contribute to neuronal damage and cognitive impairment and accelerate normal brain aging. Additionally, it also addresses the impact of antiretroviral therapy on brain aging and the biological markers associated with its occurrence. Methods: We extensively searched PubMed for English-language articles published from 2000 to 2024. The following keywords were used in the search: “HIV”, “brain”, “brain aging”, “neuroinflammation”, “HAART”, and “HAND”. This strategy yielded 250 articles for inclusion in our review. Results: A combination of blood-brain barrier dysfunction, with the direct effects of HIV on the central nervous system, chronic neuroinflammation, telomere shortening, neurogenesis impairments, and neurotoxicity associated with antiretroviral treatment (ART), alters and amplifies the mechanisms of normal brain aging. Conclusions: Current evidence suggests that HIV infection accelerates neurodegenerative processes of normal brain aging, leading to cognitive decline and structural brain changes at an earlier age than typically observed in the general population. Full article

HIV and parasite infections accelerate biological aging, resulting in immune senescence, apoptosis and cellular damage. Telomere length is considered to be one of the most effective biomarkers of biological aging. HIV and parasite infection have been reported to shorten telomere length in the host. This systematic review aimed to highlight work that explored the influence of HIV and parasite single infections and coinfection on telomere length. Using specific keywords related to the topic of interest, an electronic search of several online databases (Google Scholar, Web of Science, Scopus, Science Direct and PubMed) was conducted to extract eligible articles. The association between HIV infection or parasite infection and telomere length and the association between HIV and parasite coinfection and telomere length were assessed independently. The studies reported were mostly conducted in the European countries. Of the 42 eligible research articles reviewed, HIV and parasite single infections were independently associated with telomere length shortening. Some studies found no association between antiretroviral therapy (ART) and telomere length shortening, while others found an association between ART and telomere length shortening. No studies reported on the association between HIV and parasite coinfection and telomere length. HIV and parasite infections independently accelerate telomere length shortening and biological aging. It is possible that coinfection with HIV and parasites may further accelerate telomere length shortening; however, this is a neglected field of research with no reported studies to date. Full article

Antiretroviral therapy (ART) regimens have been shown to cause metabolic changes in people living with HIV (PLWH), predisposing them to cardiometabolic disease (CVMD). However, such evidence is less established in pregnant women living with HIV (pWLWH) on ART. Pregnancy-induced cardiometabolic risks (CMR) can predispose to unfavourable pregnancy outcomes and further persist in the postpartum period, resolve, and recur in subsequent pregnancies, or emerge as newly diagnosed chronic diseases of ageing. Therefore, this systematic review aimed at synthesizing evidence on CMR and perinatal outcomes among pWLWH in the era of ART. We considered prospective and retrospective cohorts, case-control, cross-sectional, and interventional studies published in English. Specific keywords were used to conduct a thorough literature search on PubMed-Medline and Scopus following the Preferred Reporting Items for Systematic Review and Meta-Analysis guideline. Two investigators independently screened the search outputs and reviewed full texts of potentially eligible articles. Data extraction was conducted by one investigator and verified by the second investigator. Thirty-one relevant studies conducted on 20,904 pWLWH on ART across Africa, Asia, Europe, and America were included. Studies demonstrate inconclusive findings, especially on perinatal outcomes, but significant risks of gestational hypertension and dyslipidemia were reported in pWLWH on ART compared to the control group. Therefore, future studies should focus more on these perinatal outcomes, and their impact on postpartum maternal health and growth trajectories of uninfected infants born from pWLWH who are either on ART or ART-naïve in comparison to infants born of HIV-negative mothers over the life course, especially in HIV-burdened African countries. Full article

To date, therapeutic switches are performed to reduce and prevent toxicity, improve adherence, promote virological control, and save costs. Drug switches are a daily challenge in the management of people living with HIV (PLWH), especially in those with multiple comorbidities and on polypharmacy. The objectives of this prospective analysis were: (I) to evaluate the viro-immunological efficacy of BIC/FTC/TAF in a cohort of PLWH who switched to this regimen from any other previous, at the Infectious and Tropical Diseases Unit of the Padua University Hospital; (II) to assess the impact on body weight, lipids, and renal function parameters at week 48; and (III) to evaluate daily costs changes, adherence, and the rate and causes of discontinuation of the regimen. We included all adult PLWH who switched to BIC/FTC/TAF from 1 February 2020 to 31 October 2021. We collected demographic, clinical, and laboratory data at baseline and week 48 after the switch. In addition, the estimated cART-related cost changes over the follow-up period were calculated. Over the study period, 290 individuals who switched to BIC/FTC/TAF, 76.9% were males, with a median age of 52 years, and 94.8% had an undetectable baseline HIV viremia. After a median time of 35 days (IQR: 1–55), 41 (14.1%) individuals discontinued the regimen. Factors significantly associated with discontinuation were switching from dual regimens, and neurological disorders. At week 48, we detected a significant increase in body weight, BMI, CD4 T-cell count, and CD4/CD8 ratio, and a significant reduction in triglycerides and costs; all patients had undetectable HIV RNA. Our results showed that switching to BIC/FTC/TAF may favor slightly immunological recovery and cost saving (−4.2 EUR/day from baseline to week 48, equivalent to a mean saving of 1533 EUR/year/person). The reduction in triglycerides does not appear to be clinically relevant, even if statistically significant, nor do both the increase in body weight and BMI (+1 kg and +0.29 BMI, respectively) and the increase in CD4 T-cell count (+45 cells/mmc). Further studies are needed to confirm our results. Full article

Kaposi’s sarcoma is a rare disease with four known variants: classic, epidemic, endemic and iatrogenic (transplant-related), all caused by an oncogenic virus named Human Herpes Virus 8. The viral infection in itself, along with the oncogenic properties of HHV8 and with immune system dysfunction, forms the grounds on which Kaposi’s Sarcoma may develop. Infection with HHV8 occurs through saliva via close contacts, blood, blood products, solid organ donation and, rarely, vertical transmission. Chronic inflammation and oncogenesis are promoted by a mix of viral genes that directly promote cell survival and transformation or interfere with the regular cell cycle and cell signaling (of particular note: LANA-1, v-IL6, vBCL-2, vIAP, vIRF3, vGPCR, gB, K1, K8.1, K15). The most common development sites for Kaposi’s sarcoma are the skin, mucocutaneous zones, lymph nodes and visceral organs, but it can also rarely appear in the musculoskeletal system, urinary system, endocrine organs, heart or eye. Histopathologically, spindle cell proliferation with slit-like vascular spaces, plasma cell and lymphocyte infiltrate are characteristic. The clinical presentation is heterogenic depending on the variant; some patients have indolent disease and others have aggressive disease. The treatment options include highly active antiretroviral therapy, surgery, radiation therapy, chemotherapy, and immunotherapy. A literature search was carried out using the MEDLINE/PubMed, SCOPUS and Google Scholar databases with a combination of keywords with the aim to provide critical, concise, and comprehensive insights into advances in the pathogenic mechanism of Kaposi’s sarcoma. Full article