HIV and Viral Hepatitis Prevention, Treatment and Coinfection, 2nd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Biopharmaceuticals".

Deadline for manuscript submissions: 25 June 2026 | Viewed by 1143

Special Issue Editors


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Guest Editor
Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Madrid, Spain
Interests: hepatitis C virus; HIV; infectious diseases; virology; nanomedicine; neutralizing antibody
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Madrid, Spain
Interests: HIV; hepatitis C; infectious diseases; immunology; virology; genetics; epidemiology; cirrhosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatitis C is a disease caused by HCV that infects the liver and causes inflammation. According to the WHO, 58 million people worldwide live with chronic HCV infection and more than 350,000 people die each year from liver diseases related to this virus. Despite the extraordinary efficacy of direct-acting antivirals (DAAs) against HCV infection (with cure rates over 95%), there are still limitations that need to be addressed, including the lack of access to DAAs in marginalized and at-risk populations who are potential HCV transmitters, the emergence of multidrug resistance and reinfections.

On the other hand, HIV progressively attacks and weakens the immune system, destroys CD4 cells and ultimately leads to AIDS, increasing vulnerability to opportunistic infections. According to the WHO, 37.7 million people live with HIV and approximately 600,000 people die from HIV-related causes each year. Despite the great success of combined antiretroviral therapy, in the absence of an approved and effective vaccine, there is an urgent need to develop other alternative methods of pre-exposure prophylaxis.

As HCV and HIV share transmission routes, a large proportion of HCV-infected individuals are also coinfected with HIV. HIV/HCV coinfection increases the morbidity and mortality of patients with HIV due to the more aggressive progression of fibrosis and liver cirrhosis in coinfected individuals.

For this Special Issue, we invite contributors to submit research on discovering drugs with novel mechanisms of action, developing vaccines with the capacity to generate humoral immunity (for example, stimulating naive B cells in large populations to induce broadly neutralizing antibodies based on HIV Env or HCV E2) or different formulations (i.e., microbicides), to provide effective tools in the treatment, prevention, and eradication of these viruses.

Dr. Daniel Sepúlveda-Crespo
Dr. Salvador Resino
Guest Editors

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Keywords

  • coinfection
  • drug discovery
  • HBV
  • HCV
  • HDV
  • HIV
  • neutralizing antibodies
  • prevention
  • treatment
  • vaccine

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Published Papers (1 paper)

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Research

17 pages, 2761 KB  
Article
Plasma miRNA-Metabolite Dysregulation in People with HIV with Cirrhosis Despite Successful HCV Cure
by Ana Virseda-Berdices, Raquel Behar-Lagares, Juan Berenguer, Juan González-García, Belen Requena, Oscar Brochado-Kith, Cristina Díez, Victor Hontañon, Sergio Grande-García, Carolina González-Riano, Coral Barbas, Salvador Resino, Amanda Fernández-Rodríguez, María Ángeles Jiménez-Sousa and the Marathon Study Group
Pharmaceuticals 2026, 19(1), 170; https://doi.org/10.3390/ph19010170 - 19 Jan 2026
Viewed by 641
Abstract
Background: Persistent liver pathology despite a sustained virologic response (SVR) to hepatitis C virus (HCV) therapy is a major clinical concern. This is particularly relevant for people with HIV (PWH) with HCV coinfection, a population prone to accelerated liver disease progression. This [...] Read more.
Background: Persistent liver pathology despite a sustained virologic response (SVR) to hepatitis C virus (HCV) therapy is a major clinical concern. This is particularly relevant for people with HIV (PWH) with HCV coinfection, a population prone to accelerated liver disease progression. This study aimed to characterize the plasma miRNA profile in PWH with cirrhosis one year after successful completion of HCV therapy, and to explore their relationship with metabolite alterations. Methods: This cross-sectional study enrolled 47 PWH who achieved HCV clearance with antiviral therapy. Using plasma samples collected approximately one year after completion of HCV therapy, participants were stratified into two groups based on liver stiffness measurement (LSM): compensated cirrhosis (n = 32, LSM ≥ 12.5 kPa) and non-cirrhosis (n = 15, LSM < 12.5 kPa). Plasma miRNAs and metabolites were determined using small RNA sequencing and untargeted capillary electrophoresis-mass spectrometry (CE-MS), respectively. Significantly differentially expressed (SDE) miRNAs were identified using generalized linear models (GLM) with a negative binomial distribution, and their correlation with metabolite levels was quantified using Spearman’s correlation. Results: In the cirrhosis group (n = 32), we identified a distinct signature of 15 SDE miRNAs (9 upregulated, 6 downregulated) compared to the non-cirrhotic group (n = 15), showing hsa-miR-10401-3p, hsa-miR-548ak, hsa-miR-141-3p, and hsa-miR-3940-3p the largest expression changes. miRNA-gene interaction and pathway enrichment analysis suggested that these 15 SDE miRNAs potentially regulate multiple genes involved in immune response and amino acid metabolism. In addition, correlation analyses with our metabolomic data revealed significant associations between specific SDE miRNAs and amino acids and their derivatives. Specifically, the expression of upregulated miRNAs (e.g., hsa-miR-10401-3p and hsa-miR-16-5p) was positively correlated with plasma levels of L-methionine and its derivatives, while downregulated miRNAs (e.g., hsa-miR-625-5p) were inversely correlated with L-tryptophan. Conclusions: In cirrhotic PWH with history of HCV coinfection, a distinct plasma miRNA signature linked to dysregulated amino acid metabolism is found one year after completion of HCV therapy. This underscores that the HCV cure does not equate to complete hepatic recovery, highlighting the critical need for long-term monitoring in this high-risk population. Full article
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