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Pathogens
Special Issues
New Insights into Viral Pathogenesis, Host Immune Responses and Immunotherapies
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New Insights into Viral Pathogenesis, Host Immune Responses and Immunotherapies

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: 30 October 2024 | Viewed by 3748

Special Issue Editors

Dr. Dawei Zhou

E-Mail Website
Guest Editor
Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
Interests: viral pathogenesis; virus-host interaction; immunology; epigenetics; cell signaling
Dr. Taiwei Li

E-Mail Website
Guest Editor
Seattle Children's Hospital, University of Washington, Seattle, WA 98105, USA
Interests: HIV; SARS-CoV-2 (COVID-19); viral-host interaction; anti-viral research; viral innate immunity
Dr. Theresa Chang

E-Mail Website
Guest Editor
Department of Microbiology and Molecular Genetics, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA
Interests: mucosal immunity (female reproductive tracts and GI); host–virus interaction; HIV; herpesvirus; human papillomavirus; Zika virus; SARS-CoV-2
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Viral diseases account for approximately 60% of all infectious diseases. In the landscape of viral diseases, a profound understanding of the intricate interplay between viral pathogens and the host cellular machinery is a cornerstone of the progress of basic, preclinical and clinical studies. Viral pathogenesis, elucidating the molecular mechanisms underlying viral invasion, replication, and dissemination within the host, is paramount for deciphering disease progression and transmission dynamics. Concurrently, comprehending the orchestration of host antiviral immune responses, encompassing innate and adaptive immunity, unveils the multifaceted defense mechanisms against viral infection. Harnessing the power of the immune system, antiviral immunotherapies has emerged as a frontier of unparalleled significance, from the conventional application of monoclonal antibodies and interferons to the innovative immune checkpoint blockade, which modulate immune responses to control viral spread, offering alternatives for drug-resistant viruses.

The significance of this special issue of Pathogens lies in potential breakthroughs against all types of viral threats including emerging viruses, like coronaviruses, and persistent challenges such as HIV and herpesviruses. We aim to focus on the new insights into the molecular mechanisms of viral replication, pathogenesis, antiviral innate and adaptive immune responses, as well as effective immune strategies for prevention, treatment, and control of viral diseases.

Dr. Dawei Zhou
Dr. Taiwei Li
Dr. Theresa Chang
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. Pathogens 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 2200 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

  • virus-host interaction
  • viral replication
  • viral pathogenesis
  • host immune responses
  • antiviral immunotherapies

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Published Papers (2 papers)

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Research

10 pages, 557 KiB  
Article
The Effect of Exposure to SARS-CoV-2 Vaccination and Infection on Humoral and Cellular Immunity in a Cohort of Patients with Immune-Mediated Diseases: A Pilot Study
by Giulia Anna Maria Luigia Costanzo, Giuseppina Sanna, Francesco Pes, Carla Maria Deiana, Andrea Giovanni Ledda, Andrea Perra, Vanessa Palmas, Valeria Manca, Michela Miglianti, Ferdinando Coghe, Aldo Manzin, Stefano Del Giacco, Luchino Chessa and Davide Firinu
Pathogens 2024, 13(6), 506; https://doi.org/10.3390/pathogens13060506 - 14 Jun 2024
Viewed by 909
Abstract
Immunization against COVID-19 is needed in patients with immune-mediated inflammatory diseases (IMIDs). However, data on long-term immunity kinetics remain scarce. This study aimed to compare the humoral and cellular response to COVID-19 in patients with immune-mediated inflammatory diseases (IMIDs) compared to healthy controls. [...] Read more.
Immunization against COVID-19 is needed in patients with immune-mediated inflammatory diseases (IMIDs). However, data on long-term immunity kinetics remain scarce. This study aimed to compare the humoral and cellular response to COVID-19 in patients with immune-mediated inflammatory diseases (IMIDs) compared to healthy controls. We compared the humoral and cellular response to SARS-Cov-2 elicited by vaccination and/or infection in a prospective cohort of 20 IMID patients compared with a group of 21 healthcare workers (HCWs). We assessed immunity before and after the third and fourth dose of BNT162b2 or after COVID-19 infection using quantitative IgG anti-SARS-CoV-2 Spike antibody (anti-S-IgG), neutralization assay, and specific interferon-gamma (IFN-g) release assay (IGRA). The responses were compared with those of healthy controls. The two groups were similar in age and total exposure, becoming infected for the first time, mainly after the third dose. Neutralizing antibodies and IGRA were negative in 9.5% of IMID patients but not in any HCWs. No significant difference was found between neutralization titers to BA.1 in the IMID and the HCW groups. The study highlights the SARS-CoV-2 immunological responses in healthy controls and IMID patients, suggesting that the combined stimuli of vaccination and infection in IMID patients could promote a more profound immunological response. Full article
(This article belongs to the Special Issue New Insights into Viral Pathogenesis, Host Immune Responses and Immunotherapies)
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Figure 1

Figure 1
<p>Study design. Legend: IMIDs: immune-mediated inflammatory diseases; Neutralizing ab: serum neutralizing antibody titer assessed by SARS-CoV-2 microneutralization assay (90% protective activity of neutralizing Ab against the CPE induced by the virus); IGRA: Interferon-gamma (IFN-g) release assay to SARS-CoV-2 Spike protein (Wuhan/Hu-1/2019 and 20J/501Y.V3 “gamma” variant).</p> Full article ">
22 pages, 3751 KiB  
Article
Immune Responses in Oral Papillomavirus Clearance in the MmuPV1 Mouse Model
by Sarah A. Brendle, Jingwei J. Li, Vonn Walter, Todd D. Schell, Michael Kozak, Karla K. Balogh, Song Lu, Neil D. Christensen, Yusheng Zhu, Karam El-Bayoumy and Jiafen Hu
Pathogens 2023, 12(12), 1452; https://doi.org/10.3390/pathogens12121452 - 14 Dec 2023
Cited by 3 | Viewed by 2339
Abstract
Human papillomavirus (HPV)-induced oropharyngeal cancer now exceeds HPV-induced cervical cancer, with a noticeable sex bias. Although it is well established that women have a more proficient immune system, it remains unclear whether immune control of oral papillomavirus infections differs between sexes. In the [...] Read more.
Human papillomavirus (HPV)-induced oropharyngeal cancer now exceeds HPV-induced cervical cancer, with a noticeable sex bias. Although it is well established that women have a more proficient immune system, it remains unclear whether immune control of oral papillomavirus infections differs between sexes. In the current study, we use genetically modified mice to target CCR2 and Stat1 pathways, with the aim of investigating the role of both innate and adaptive immune responses in clearing oral papillomavirus, using our established papillomavirus (MmuPV1) infection model. Persistent oral MmuPV1 infection was detected in Rag1ko mice with T and B cell deficiencies. Meanwhile, other tested mice were susceptible to MmuPV1 infections but were able to clear the virus. We found sex differences in key myeloid cells, including macrophages, neutrophils, and dendritic cells in the infected tongues of wild type and Stat1ko mice but these differences were not observed in CCR2ko mice. Intriguingly, we also observed a sex difference in anti-MmuPV1 E4 antibody levels, especially for two IgG isotypes: IgG2b and IgG3. However, we found comparable numbers of interferon-gamma-producing CD8 T cells stimulated by E6 and E7 in both sexes. These findings suggest that males and females may use different components of innate and adaptive immune responses to control papillomavirus infections in the MmuPV1 mouse model. The observed sex difference in immune responses, especially in myeloid cells including dendritic cell (DC) subsets, may have potential diagnostic and prognostic values for HPV-associated oropharyngeal cancer. Full article
(This article belongs to the Special Issue New Insights into Viral Pathogenesis, Host Immune Responses and Immunotherapies)
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Figure 1

Figure 1
<p>Viral DNA in oral swabs and viral transcripts detected in the infected tongues. We followed viral replication in the infected mice by collecting longitudinal oral swabs and analyzed viral DNA by qPCR. Significantly higher levels of viral DNA were detected in the oral swabs of Rag1ko mice when compared to the infected B6 mice ((<b>A</b>), * <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test) at different time points post-viral infection. No viral DNA was detected in B6 mice at week six post-viral infection. The infected tongues were harvested for viral RNA analysis by qRT-PCR at week four post-viral infection. Viral RNA transcripts were detected in some infected tongues of different mouse strains (<a href="#pathogens-12-01452-t002" class="html-table">Table 2</a>). While more than half of B6 and Rag1ko mice were positive for viral transcripts, two CCR2ko and four Stat1ko mice (out of six each) had very low levels of viral RNA at week four post-viral infection. No significant difference was found between the different groups of animals as well as different sexes ((<b>B</b>), <span class="html-italic">p</span> &gt; 0.05, the Kruskal–Wallis test).</p> Full article ">Figure 2
<p>Immune cell profiling using multi-color flow cytometry assay. The schematic flow chart of gating different immune cell populations from flow cytometry assays (<b>A</b>). Viable single leukocytes (CD45<sup>+</sup>) from either spleens or tongues were gated for subset discrimination. Total dendritic cells (CD11c<sup>+</sup>F4-80<sup>−</sup>) by exclusion of macrophage (F4-80<sup>+</sup>) cells were further analyzed to determine two dendritic cell populations including cDC1 (CD11b<sup>−</sup>CD11c<sup>+</sup>) and cDC2 (CD11b<sup>+</sup>CD11c<sup>+</sup>). Higher but not significantly higher numbers of cDC2 were found in both B6 and CCR2ko females (based on live cell population) when compared to corresponding males ((<b>B</b>), <span class="html-italic">p</span> &gt; 0.05, Mann–Whitney rank sum test). Dermal DCs (CD205<sup>+</sup>) of total DCs and plasmacytoid DCs (CD11b<sup>−</sup>SiglecH<sup>+</sup>) were further determined. Macrophages (F4-80<sup>+</sup>) and granulocytes (Ly6G<sup>+</sup>) were identified within the CD11b<sup>+</sup> cell population. Significantly higher levels of dermal DCs (F4-80<sup>−</sup>CD205<sup>+</sup>) were also found in female CCR2ko mice when compared to corresponding B6 and Stat1ko female mice as well as CCR2ko males ((<b>C</b>), * <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). No significant difference in pDCs (CD11b<sup>−</sup>SiglecH<sup>+</sup>) was found among all groups even though higher but not significantly higher numbers of pDCs were found in infected Stat1ko males ((<b>D</b>), <span class="html-italic">p</span> &gt; 0.05, Mann–Whitney rank sum test).</p> Full article ">Figure 3
<p>Sex difference in local macrophages and granulocytes was found. Significantly higher levels of macrophages in spleen of both male and female Stat1ko mice (<b>A</b>) when compared to corresponding B6 and CCR2ko (* for male, # for female, <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). More Ly6G<sup>+</sup> cells in the spleen were found in Stat1ko females when compared to the corresponding males. Interestingly, higher levels of macrophages were found in infected tongues (<b>B</b>) of B6 female mice when compared to corresponding B6 males ((<b>B</b>), * <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). More Ly6G<sup>+</sup> granulocytes in the spleen were found in Stat1ko females when compared to the corresponding males ((<b>C</b>), * <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). A sex difference was not found in the infected tongue of B6 mice for Ly6G<sup>+</sup> granulocytes ((<b>D</b>), * <span class="html-italic">p</span> &gt; 0.05, Mann–Whitney rank sum test). Significantly higher levels of Ly6G<sup>+</sup> granulocytes were found in CCR2ko males when compared to corresponding B6 females (<span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test).</p> Full article ">Figure 4
<p>No difference in NK cells was found among different mouse strains. Comparable levels of NK cells were found in infected tongues of B6, CCR2, and Stat1ko mice. Neither sex difference nor strain difference was observed in NK cells in Stat1ko or CCR2ko mice (<span class="html-italic">p</span> &gt; 0.05, Mann–Whitney rank sum test).</p> Full article ">Figure 5
<p>A sex difference in anti-MmuPV1 E4 IgG and isotypes was found. Anti-MmuPV1 E4 IgG antibodies in B6, CCR2ko, and Stat1ko mice post-infection. Significantly higher levels of antibodies against E4 (IgG) were found in females when compared with those of corresponding males of all tested mouse strains ((<b>A</b>), * <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). Significantly lower levels of E4 IgG were found in B6 females when compared to that of CCR2ko and Stat1ko females ((<b>A</b>), # <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test). Significantly higher levels of antibodies were found in females of CCR2ko for IgG3 (<b>E</b>) but not IgG1 (<b>B</b>), IgG2b (<b>C</b>), and IgG2c (<b>D</b>) isotypes. Significantly lower levels of E4 IgG3 were found in B6 females when compared to that of CCR2ko and Stat1ko females ((<b>E</b>), # <span class="html-italic">p</span> &lt; 0.05, Mann–Whitney rank sum test, * for B6 vs. stat1ko females).</p> Full article ">Figure 6
<p>Viral transcripts (<b>A</b>) in the infected tongues and anti-MmuPV1 E4 IgG (<b>B</b>,<b>C</b>) in the sera of MmuPV1-infected BALB/C and FVB mice. BALB/C and FVB mice were tested for infection in the tongue. Similar levels of viral transcripts were found in both male and female mice for both strains (<b>A</b>). Similar to what we observed in other mice, significantly higher levels of anti-MmuPV1 E4 isotype IgG3 were found in females of BALB/c ((<b>B</b>), * <span class="html-italic">p</span> = 0.0395, Mann–Whitney rank sum test) and FVB ((<b>C</b>), * <span class="html-italic">p</span> &lt; 0.01, Mann–Whitney rank sum test) when compared to the corresponding males. No significant difference was found in anti-MmuPV1 E4 isotype IgM between mouse strains.</p> Full article ">Figure 7
<p>Cytotoxic T cells against anti-MmuPV1 E6 and E7 were detected in infected B6 mice. Anti-MmuPV1 CD8 T cells (PE/CY7-tagged) that release interferon gamma (APC tagged) after MmuPV1 E6/90-99 (KNIVFVTVR) (<b>A</b>), E7/69-77 (VLRFIIVTG) (<b>B</b>), or mock (<b>C</b>) peptide stimulation in splenocytes from both male and female B6 mice. Significantly higher numbers of CD8 T cells to E6/90-99 were detected when compared to E7 and mock-infected B6 mice ((<b>D</b>), * <span class="html-italic">p</span> &lt; 0.05 vs. mock, the Kruskal–Wallis test). When separating the data based on sex, a significant difference was found in male B6 mice to E6/90-99 ((<b>E</b>), * <span class="html-italic">p</span> &lt; 0.05 vs. mock, the Kruskal–Wallis test).</p> Full article ">Figure 8
<p>The schematic model for immune responses during viral clearance in the oral MmuPV1 infection mouse model. Several key innate immune cells that are involved in viral clearance of males (M) and females (F) are shown. Both Stat1 and CCR2ko mice showed increased dermal dendritic cell population in the infected tongues when compared with B6 mice. In contrast, CCR2ko male mice recruited increased numbers of ly6G+ granulocytes to the infected tongues than corresponding B6 and Stat1ko males. A similar pattern of sex difference in macrophages and neutrophils was found in B6 and Stat1ko mice. Both sexes elicited similar levels of CD8 T-cell-mediated immune responses after MmuPV1 infection. Intriguingly, significantly higher levels of anti-E4 IgG (especially IgG3 subtype) were found in females irrespective of mouse strain with increased levels in both CCR2 and Stat1ko female mice. Symbols: “&gt;” higher; “&lt;” lower; and “=” comparable levels of immune cell population/responses were detected between males (M) and females (F).</p> Full article ">
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