Host-Virus Interactions in Viral Infectious Diseases

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 26692

Special Issue Editor


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Guest Editor
1. Department of Microbiology and Pathology, University Center for Health Science (CUCS), University of Guadalajara, Guadalajara 44340, Mexico
2. Center for Infectious Disease and Vaccine Research, La Jolla Institute for Immunology, La Jolla, CA 92037, USA
Interests: dengue; Zika; SARS-CoV-2
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Special Issue Information

Dear Colleagues,

The aim of this Special Issue to focus on host–virus interactions in viral infectious diseases. The world has recently been confronted with emerging and re-emerging zoonotic viruses, in particular recently emerging diseases such as monkeypox, COVID-19, acute hepatitis in children, Zika and Dengue. This Special Issue will address topics including but not limited to the following: virus–host interactions, antiviral responses, host immunity, viral vaccine, and viral pathogenesis.

The identification of host factors is critical for viral pathogenesis. Understanding how viruses replicate and infect is essential in order to development new therapies and vaccines, and to improve our understanding of virus-induced diseases.

This Special Issue invites all types of manuscripts, including research articles, reviews and short communications.

We look forward to your submissions on the topic of Host-Virus Interactions in Viral Infectious Diseases.

Dr. Jose Angel Regla Nava
Guest Editor

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Keywords

  • virus infection
  • viral pathogenesis
  • host responses
  • infectious diseases
  • antiviral immunity
  • host immune
  • viral immune evasion
  • emerging viruses
  • virus–host interactions
  • antiviral responses
  • restriction factors
  • zoonotic viruses
  • viral vaccines

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Published Papers (7 papers)

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Research

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16 pages, 2669 KiB  
Article
Characterization of Viral Interference in Aedes albopictus C6/36 Cells Persistently Infected with Dengue Virus 2
by Aurora Montsserrat González-Flores, Mariana Salas-Benito, Victor Hugo Rosales-García, Paola Berenice Zárate-Segura, Rosa María Del Ángel, Mónica Ascención De Nova-Ocampo and Juan Santiago Salas-Benito
Pathogens 2023, 12(9), 1135; https://doi.org/10.3390/pathogens12091135 - 6 Sep 2023
Cited by 2 | Viewed by 2767
Abstract
Arboviruses are an important group of pathogens that cause diseases of medical and veterinary concern worldwide. The interactions of these viruses with their host cells are complex, and frequently, the coexistence of two different viruses in the same cell results in the inhibition [...] Read more.
Arboviruses are an important group of pathogens that cause diseases of medical and veterinary concern worldwide. The interactions of these viruses with their host cells are complex, and frequently, the coexistence of two different viruses in the same cell results in the inhibition of replication in one of the viruses, which is a phenomenon called viral interference. This phenomenon can be exploited to develop antiviral strategies. Insect cell lines persistently infected with arboviruses are useful models with which to study viral interference. In this work, a model of C6/36-HT cells (from Aedes albopictus mosquitoes) persistently infected with Dengue virus, serotype 2, was used. Viral interference was evaluated via plaque and flow cytometry assays. The presence of heterotypic interference against the other serotypes of the same virus and homologous interference against yellow fever virus was determined; however, this cell line did not display heterologous viral interference against Sindbis virus. The mechanisms responsible for viral interference have not been fully elucidated, but small RNAs could be involved. However, the silencing of Ago3, a key protein in the genome-derived P-element-induced wimpy testis pathway, did not alter the viral interference process, suggesting that viral interference occurs independent of this pathway. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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Review

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23 pages, 456 KiB  
Review
Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs
by Matloob Husain
Pathogens 2024, 13(2), 127; https://doi.org/10.3390/pathogens13020127 - 29 Jan 2024
Cited by 2 | Viewed by 3091
Abstract
Influenza virus has been one of the most prevalent and researched viruses globally. Consequently, there is ample information available about influenza virus lifecycle and pathogenesis. However, there is plenty yet to be known about the determinants of influenza virus pathogenesis and disease severity. [...] Read more.
Influenza virus has been one of the most prevalent and researched viruses globally. Consequently, there is ample information available about influenza virus lifecycle and pathogenesis. However, there is plenty yet to be known about the determinants of influenza virus pathogenesis and disease severity. Influenza virus exploits host factors to promote each step of its lifecycle. In turn, the host deploys antiviral or restriction factors that inhibit or restrict the influenza virus lifecycle at each of those steps. Two broad categories of host restriction factors can exist in virus-infected cells: (1) encoded by the interferon-stimulated genes (ISGs) and (2) encoded by the constitutively expressed genes that are not stimulated by interferons (non-ISGs). There are hundreds of ISGs known, and many, e.g., Mx, IFITMs, and TRIMs, have been characterized to restrict influenza virus infection at different stages of its lifecycle by (1) blocking viral entry or progeny release, (2) sequestering or degrading viral components and interfering with viral synthesis and assembly, or (3) bolstering host innate defenses. Also, many non-ISGs, e.g., cyclophilins, ncRNAs, and HDACs, have been identified and characterized to restrict influenza virus infection at different lifecycle stages by similar mechanisms. This review provides an overview of those ISGs and non-ISGs and how the influenza virus escapes the restriction imposed by them and aims to improve our understanding of the host restriction mechanisms of the influenza virus. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
24 pages, 1724 KiB  
Review
Herpesviruses and SARS-CoV-2: Viral Association with Oral Inflammatory Diseases
by Jonathan M. Banks, Kristelle J. Capistrano, Daniela A. Brandini, Filza Zaidi, Pari Thakkar, Rani Rahat, Joel Schwartz and Afsar R. Naqvi
Pathogens 2024, 13(1), 58; https://doi.org/10.3390/pathogens13010058 - 7 Jan 2024
Cited by 5 | Viewed by 4926
Abstract
The oral cavity is a niche for diverse microbes, including viruses. Members of the Herpesviridae family, comprised of dsDNA viruses, as well as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an ssRNA virus, are among the most prevalent viruses infecting the oral cavity, [...] Read more.
The oral cavity is a niche for diverse microbes, including viruses. Members of the Herpesviridae family, comprised of dsDNA viruses, as well as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an ssRNA virus, are among the most prevalent viruses infecting the oral cavity, and they exhibit clinical manifestations unique to oral tissues. Viral infection of oral mucosal epithelia triggers an immune response that results in prolonged inflammation. The clinical and systemic disease manifestations of HHV have been researched extensively, and several recent studies have illuminated the relationship between HHV and oral inflammatory diseases. Burgeoning evidence suggests the oral manifestation of SARS-CoV-2 infection includes xerostomia, dysgeusia, periodontal disease, mucositis, and opportunistic viral and bacterial infections, collectively described as oral post-acute sequelae of COVID-19 (PASC). These diverse sequelae could be a result of intensified immune responses initially due to the copious production of proinflammatory cytokines: the so-called “cytokine storm syndrome”, facilitating widespread oral and non-oral tissue damage. This review explores the interplay between HHV, SARS-CoV-2, and oral inflammatory diseases such as periodontitis, endodontic disease, and peri-implantitis. Additionally, the review discusses proper diagnostic techniques for identifying viral infection and how viral diagnostics can lead to improved overall patient health. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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16 pages, 3021 KiB  
Review
Cell Fractionation and the Identification of Host Proteins Involved in Plant–Virus Interactions
by Amany E. Gomaa, Kaoutar El Mounadi, Eric Parperides and Hernan Garcia-Ruiz
Pathogens 2024, 13(1), 53; https://doi.org/10.3390/pathogens13010053 - 5 Jan 2024
Cited by 1 | Viewed by 2660
Abstract
Plant viruses depend on host cellular factors for their replication and movement. There are cellular proteins that change their localization and/or expression and have a proviral role or antiviral activity and interact with or target viral proteins. Identification of those proteins and their [...] Read more.
Plant viruses depend on host cellular factors for their replication and movement. There are cellular proteins that change their localization and/or expression and have a proviral role or antiviral activity and interact with or target viral proteins. Identification of those proteins and their roles during infection is crucial for understanding plant–virus interactions and to design antiviral resistance in crops. Important host proteins have been identified using approaches such as tag-dependent immunoprecipitation or yeast two hybridization that require cloning individual proteins or the entire virus. However, the number of possible interactions between host and viral proteins is immense. Therefore, an alternative method is needed for proteome-wide identification of host proteins involved in host–virus interactions. Here, we present cell fractionation coupled with mass spectrometry as an option to identify protein–protein interactions between viruses and their hosts. This approach involves separating subcellular organelles using differential and/or gradient centrifugation from virus-free and virus-infected cells (1) followed by comparative analysis of the proteomic profiles obtained for each subcellular organelle via mass spectrometry (2). After biological validation, prospect host proteins with proviral or antiviral roles can be subject to fundamental studies in the context of basic biology to shed light on both virus replication and cellular processes. They can also be targeted via gene editing to develop virus-resistant crops. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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18 pages, 4252 KiB  
Review
Host and HBV Interactions and Their Potential Impact on Clinical Outcomes
by Alexis Jose-Abrego, Sonia Roman, Saul Laguna-Meraz and Arturo Panduro
Pathogens 2023, 12(9), 1146; https://doi.org/10.3390/pathogens12091146 - 8 Sep 2023
Cited by 7 | Viewed by 3234
Abstract
Hepatitis B virus (HBV) is a challenge for global health services, affecting millions and leading thousands to end-stage liver disease each year. This comprehensive review explores the interactions between HBV and the host, examining their impact on clinical outcomes. HBV infection encompasses a [...] Read more.
Hepatitis B virus (HBV) is a challenge for global health services, affecting millions and leading thousands to end-stage liver disease each year. This comprehensive review explores the interactions between HBV and the host, examining their impact on clinical outcomes. HBV infection encompasses a spectrum of severity, ranging from acute hepatitis B to chronic hepatitis B, which can potentially progress to cirrhosis and hepatocellular carcinoma (HCC). Occult hepatitis B infection (OBI), characterized by low HBV DNA levels in hepatitis B surface antigen-negative individuals, can reactivate and cause acute hepatitis B. HBV genotyping has revealed unique geographical patterns and relationships with clinical outcomes. Moreover, single nucleotide polymorphisms (SNPs) within the human host genome have been linked to several clinical outcomes, including cirrhosis, HCC, OBI, hepatitis B reactivation, and spontaneous clearance. The immune response plays a key role in controlling HBV infection by eliminating infected cells and neutralizing HBV in the bloodstream. Furthermore, HBV can modulate host metabolic pathways involved in glucose and lipid metabolism and bile acid absorption, influencing disease progression. HBV clinical outcomes correlate with three levels of viral adaptation. In conclusion, the clinical outcomes of HBV infection could result from complex immune and metabolic interactions between the host and HBV. These outcomes can vary among populations and are influenced by HBV genotypes, host genetics, environmental factors, and lifestyle. Understanding the degrees of HBV adaptation is essential for developing region-specific control and prevention measures. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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23 pages, 1272 KiB  
Review
Human Monkeypox: A Comprehensive Overview of Epidemiology, Pathogenesis, Diagnosis, Treatment, and Prevention Strategies
by Diana Emilia Martínez-Fernández, David Fernández-Quezada, Fidel Antonio Guadalupe Casillas-Muñoz, Francisco Josué Carrillo-Ballesteros, Ana Maria Ortega-Prieto, Jose M. Jimenez-Guardeño and Jose Angel Regla-Nava
Pathogens 2023, 12(7), 947; https://doi.org/10.3390/pathogens12070947 - 18 Jul 2023
Cited by 13 | Viewed by 5574
Abstract
Monkeypox virus (MPXV) is an emerging zoonotic virus that belongs to the Orthopoxvirus genus and presents clinical symptoms similar to those of smallpox, such as fever and vesicular–pustular skin lesions. However, the differential diagnosis between smallpox and monkeypox is that smallpox does not [...] Read more.
Monkeypox virus (MPXV) is an emerging zoonotic virus that belongs to the Orthopoxvirus genus and presents clinical symptoms similar to those of smallpox, such as fever and vesicular–pustular skin lesions. However, the differential diagnosis between smallpox and monkeypox is that smallpox does not cause lymphadenopathy but monkeypox generates swelling in the lymph nodes. Since the eradication of smallpox, MPXV has been identified as the most common Orthopoxvirus to cause human disease. Despite MPXV being endemic to certain regions of Africa, the current MPXV outbreak, which began in early 2022, has spread to numerous countries worldwide, raising global concern. As of the end of May 2023, over 87,545 cases and 141 deaths have been reported, with most cases identified in non-endemic countries, primarily due to human-to-human transmission. To better understand this emerging threat, this review presents an overview of key aspects of MPXV infection, including its animal reservoirs, modes of transmission, animal models, epidemiology, clinical and immunological features, diagnosis, treatments, vaccines, and prevention strategies. The material presented here provides a comprehensive understanding of MPXV as a disease, while emphasizing the significance and unique characteristics of the 2022 outbreak. This offers valuable information that can inform future research and aid in the development of effective interventions. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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15 pages, 1175 KiB  
Review
Tight Junctions, the Key Factor in Virus-Related Disease
by Guofei Ding, Qingyuan Shao, Haiyan Yu, Jiaqi Liu, Yingchao Li, Bin Wang, Haotian Sang, Dexin Li, Aiying Bing, Yanmeng Hou and Yihong Xiao
Pathogens 2022, 11(10), 1200; https://doi.org/10.3390/pathogens11101200 - 18 Oct 2022
Cited by 10 | Viewed by 2891
Abstract
Tight junctions (TJs) are highly specialized membrane structural domains that hold cells together and form a continuous intercellular barrier in epithelial cells. TJs regulate paracellular permeability and participate in various cellular signaling pathways. As physical barriers, TJs can block viral entry into host [...] Read more.
Tight junctions (TJs) are highly specialized membrane structural domains that hold cells together and form a continuous intercellular barrier in epithelial cells. TJs regulate paracellular permeability and participate in various cellular signaling pathways. As physical barriers, TJs can block viral entry into host cells; however, viruses use a variety of strategies to circumvent this barrier to facilitate their infection. This paper summarizes how viruses evade various barriers during infection by regulating the expression of TJs to facilitate their own entry into the organism causing infection, which will help to develop drugs targeting TJs to contain virus-related disease. Full article
(This article belongs to the Special Issue Host-Virus Interactions in Viral Infectious Diseases)
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