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Viruses
Special Issues
Viral Infections in Immunocompromised Hosts
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Viral Infections in Immunocompromised Hosts

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 3393

Special Issue Editors

Dr. Dora Ho

E-Mail Website
Guest Editor
Division of Infectious Diseases & Geographic Medicine, School of Medicine, Stanford University, Stanford, CA, USA
Interests: immunocompromised hosts; transplant; cancer; viral infections; fungal infections
Dr. Ralph Tayyar

E-Mail Website
Co-Guest Editor
Division of Allergy & Infectious Diseases, University of Washington, Seattle, WA, USA
Interests: immunocompromised infectious diseases; transplant; antimicrobial stewardship; viral infections; fungal infections

Special Issue Information

Dear Colleagues,

Immunocompromised hosts, including those with stem cell transplantation, solid organ transplantation, malignancies, or inborn/iatrogenic immunodeficiencies, are at increased risk for infectious complications. Among various groups of pathogens, viruses continue to cause significant morbidities and mortalities in immunocompromised patients despite recent advances in diagnostic and treatment modalities for viral infections. From herpesviruses, respiratory viruses, and polyomaviruses to viruses that cause diarrheal syndromes, therapeutic options remain limited either due to low efficacy, undesirable toxicity profile, or both. Distinguishing between “benign” viral reactivation and clinically significant viral disease is another major challenge for physicians that care for such immunocompromised patients.

To provide a forum of expert opinions and showcase the latest developments in this field, this Special Issue of Viruses is devoted to “Viral Infections in the Immunocompromised Hosts”. We welcome submission of reviews and original research articles for this Special Issue focusing on the diagnostics, management, and treatment of viral infections in immunocompromised hosts. Discussion on the immunology aspect of viral infections is also welcome.

Dr. Dora Ho
Dr. Ralph Tayyar
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • viral infections
  • herpesviruses
  • respiratory viruses
  • polyomaviruses
  • viral diarrheal syndromes
  • immunocompromised hosts
  • transplant infectious diseases

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Published Papers (2 papers)

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Research

10 pages, 1347 KiB  
Article
Association between Respiratory Virus Infection and Development of De Novo Donor-Specific Antibody in Lung Transplant Recipients
by Anoma Nellore, Julie Houp, John T. Killian, Ajit P. Limaye and Cynthia E. Fisher
Viruses 2024, 16(10), 1574; https://doi.org/10.3390/v16101574 - 5 Oct 2024
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Abstract
Chronic lung allograft dysfunction (CLAD) is the most common cause of long-term lung allograft failure. Several factors, including respiratory virus infection (RVI), have been associated with CLAD development, but the underlying mechanisms of these associations are not well understood. We hypothesize that RVI [...] Read more.
Chronic lung allograft dysfunction (CLAD) is the most common cause of long-term lung allograft failure. Several factors, including respiratory virus infection (RVI), have been associated with CLAD development, but the underlying mechanisms of these associations are not well understood. We hypothesize that RVI in lung transplant recipients elicits the development of donor-specific antibodies (DSAs), thus providing a mechanistic link between RVI and CLAD development. To test this hypothesis, we retrospectively evaluated for the presence of HLA antibodies in a cohort of lung transplant recipients with symptomatic RVI within the first four months post-transplant using sera at two time points (at/directly after the transplant and following RVI) and time-matched controls without RVI (post-transplant). We found a trend toward the development of de novo DSAs in those with symptomatic RVI versus controls [6/21 (29%) vs. 1/21 (5%), respectively, p = 0.09]. No cases or controls had DSA at baseline. We also found increased rates of CLAD and death among those who developed class II DSA versus those who did not (CLAD: 5/7 (71.4%) vs. 19/34 (54.3%), death: 5/7 (71.4%) vs. 17/35 (48.6%)). Prospective studies evaluating the temporal development of DSA after RVI in lung transplant patients and the subsequent outcomes are warranted. Full article
(This article belongs to the Special Issue Viral Infections in Immunocompromised Hosts)
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24 pages, 5701 KiB  
Article
Cytokine Dynamics and Herpesvirus Interactions in Pediatric Liver and Kidney Transplant Recipients: The Distinct Behavior of HCMV, HHV6, HHV7 and EBV
by Yessica Sánchez-Ponce, Juan Rafael Murillo-Eliosa, Abigail Morales-Sanchez and Ezequiel M. Fuentes-Pananá
Viruses 2024, 16(7), 1067; https://doi.org/10.3390/v16071067 - 2 Jul 2024
Viewed by 1970
Abstract
Pediatric solid organ transplant (SOT) recipients face a challenging balance between immunosuppression and graft rejection. While Epstein–Barr Virus (EBV) and cytomegalovirus (HCMV) are known contributors to post-transplant lymphoproliferative disease and graft rejection, respectively, the roles of herpesvirus 6 and 7 (HHV6 and HHV7) [...] Read more.
Pediatric solid organ transplant (SOT) recipients face a challenging balance between immunosuppression and graft rejection. While Epstein–Barr Virus (EBV) and cytomegalovirus (HCMV) are known contributors to post-transplant lymphoproliferative disease and graft rejection, respectively, the roles of herpesvirus 6 and 7 (HHV6 and HHV7) and the impact of these herpesviruses on cytokine levels remain unclear, leading to gaps in clinical practice. In this associative study, we measured 17 cytokines using a Bio-Plex assay in a meticulously curated plasma sample pool (N = 158) from pediatric kidney and liver transplant recipients over a one-year follow-up period. The samples included virus-negative and virus-positive cases, either individually or in combination, along with episodes of graft rejection. We observed that the elevation of IL-4, IL-8, and IL-10 correlated with graft rejection. These cytokines were elevated in samples where HCMV or HHV6 were detected alone or where EBV and HHV7 were co-detected. Interestingly, latent EBV, when detected independently, exhibited an immunomodulatory effect by downregulating cytokine levels. However, in co-detection scenarios with β-herpesviruses, EBV transitioned to a lytic state, also associating with heightened cytokinemia and graft rejection. These findings highlight the complex interactions between the immune response and herpesviruses in transplant recipients. The study advocates for enhanced monitoring of not only EBV and HCMV but also HHV6 and HHV7, providing valuable insights for improved risk assessment and targeted interventions in pediatric SOT recipients. Full article
(This article belongs to the Special Issue Viral Infections in Immunocompromised Hosts)
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