In Memory of Jianguo Wu

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 14858

Special Issue Editors


E-Mail Website
Guest Editor
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430071, China
Interests: viral infection and replication; immune escape; inflammation
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China
Interests: HBV; EV71; ZIKA; inflammation; antiviral drugs
School of Basic Medical Sciences, Wuhan University, Wuhan 430072, China
Interests: HIV infection; persistent infection; viral infection and immune dysfunction; HIV biology; retrovirology

E-Mail
Guest Editor
Department of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: molecular diagnostics; real-time PCR; point-of-care test; virology; virus-host interaction; pathogen surveillance; molecular epidemiology; emerging viruses
Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Guangzhou 510632, China
Interests: antiviral innate immune responses; inflammatory cytokines; inflammasome; oncolytic virus

Special Issue Information

Dear Colleagues,

Prof. Jianguo Wu’s contributions to Medical Virology were both significant and wide-ranging. He and his group at Wuhan University and Jinan University uncovered multiple important pathological mechanisms during the infectious diseases of several medical viruses, including HBV, HCV, HIV, EV71, DENV, ZIKV, SARS, and SARS-CoV-2. His pathological studies identified many key virus and host factors that dominate the inflammatory responses, immune regulation, or viral replication during viral infections. In addition to infection pathology, he was also responsible for significant achievements in the fields of virus epidemiology, vaccines, antiviral therapies, tumor immunology, and so on.

Sadly, Prof. Jianguo Wu passed away in October 2022. We miss his generosity in sharing reagents and methods and would like to use this opportunity to commemorate his disposition in sharing new ideas and participating in collaborative research studies. In honor of his work and scientific legacy, Viruses has set up this Special Issue which will contain articles by those who knew and worked with Wu and will cover different aspects of medical virology.

Prof. Dr. Yingle Liu
Dr. Kailang Wu
Dr. Yong Feng
Dr. Weiyong Liu
Dr. Yongkui Li
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

  • antiviral innate immunity 
  • inflammatory network 
  • viral pathogenicity 
  • inflammasome 
  • infection innovation

Published Papers (9 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review, Other

7 pages, 4363 KiB  
Editorial
In Memory of the Virologist Jianguo Wu, 1957–2022
by Ge Yang, Zhaoyang Yue, Pan Pan and Yongkui Li
Viruses 2023, 15(8), 1754; https://doi.org/10.3390/v15081754 - 17 Aug 2023
Viewed by 889
Abstract
It is with deep sorrow that we mourn the passing of the virologist Professor Jianguo Wu [...] Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

Research

Jump to: Editorial, Review, Other

15 pages, 3645 KiB  
Article
The Interaction between SARS-CoV-2 Nucleocapsid Protein and UBC9 Inhibits MAVS Ubiquitination by Enhancing Its SUMOylation
by Congcong Huang, Yiping Yin, Pan Pan, Yanping Huang, Siwei Chen, Junkai Chen, Ju Wang, Guoqing Xu, Xuan Tao, Xiao Xiao, Jian Li, Jing Yang, Zhixiong Jin, Bei Li, Zhaohui Tong, Weixing Du, Long Liu and Zhixin Liu
Viruses 2023, 15(12), 2304; https://doi.org/10.3390/v15122304 - 24 Nov 2023
Cited by 1 | Viewed by 1483
Abstract
Severe COVID-19 patients exhibit impaired IFN-I response due to decreased IFN-β production, allowing persistent viral load and exacerbated inflammation. While the SARS-CoV-2 nucleocapsid (N) protein has been implicated in inhibiting innate immunity by interfering with IFN-β signaling, the specific underlying mechanism still needs [...] Read more.
Severe COVID-19 patients exhibit impaired IFN-I response due to decreased IFN-β production, allowing persistent viral load and exacerbated inflammation. While the SARS-CoV-2 nucleocapsid (N) protein has been implicated in inhibiting innate immunity by interfering with IFN-β signaling, the specific underlying mechanism still needs further investigation for a comprehensive understanding. This study reveals that the SARS-CoV-2 N protein enhances interaction between the human SUMO-conjugating enzyme UBC9 and MAVS. Increased MAVS-UBC9 interaction leads to enhanced SUMOylation of MAVS, inhibiting its ubiquitination, resulting in the inhibition of phosphorylation events involving IKKα, TBK1, and IRF3, thus disrupting IFN-β signaling. This study highlights the role of the N protein of SARS-CoV-2 in modulating the innate immune response by affecting the MAVS SUMOylation and ubiquitination processes, leading to inhibition of the IFN-β signaling pathway. These findings shed light on the complex mechanisms utilized by SARS-CoV-2 to manipulate the host’s antiviral defenses and provide potential insights for developing targeted therapeutic strategies against severe COVID-19. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

16 pages, 20427 KiB  
Article
Umbilical Cord Mesenchymal-Stem-Cell-Derived Exosomes Exhibit Anti-Oxidant and Antiviral Effects as Cell-Free Therapies
by Yi Meng, Chengcheng Li, Yicong Liang, Yu Jiang, Haonan Zhang, Jianhua Ouyang, Wen Zhang, Rumei Deng, Qiuping Tan, Xiaolan Yu and Zhen Luo
Viruses 2023, 15(10), 2094; https://doi.org/10.3390/v15102094 - 15 Oct 2023
Viewed by 1587
Abstract
The oxidative stress induced by the accumulation of reactive oxygen species (ROS) can lead to cell aging and death. Equally, the skeletal muscle usually hosts enteroviral persistent infection in inflammatory muscle diseases. As excellent bioactive products, the exosomes derived from umbilical cord mesenchymal [...] Read more.
The oxidative stress induced by the accumulation of reactive oxygen species (ROS) can lead to cell aging and death. Equally, the skeletal muscle usually hosts enteroviral persistent infection in inflammatory muscle diseases. As excellent bioactive products, the exosomes derived from umbilical cord mesenchymal stem cells (ucMSCs) have been proven to be safe and have low immunogenicity with a potential cell-free therapeutic function. Here, exosomes derived from ucMSCs (ucMSC-EXO) were extracted and characterized. In a model of oxidative damage to skin fibroblasts (HSFs) under exposure to H2O2, ucMSC-EXO had an observable repairing effect for the HSFs suffering from oxidative damage. Furthermore, ucMSC-EXO inhibited mitogen-activated protein kinases (MAPK), c-Jun N-terminal kinase (JNK), and nuclear factor kappa-B (NF-κB) signaling pathways, thereby promoting p21 protein expression while decreasing lamin B1 protein expression, and finally alleviated oxidative stress-induced cell damage and aging. In a model of rhabdomyosarcoma (RD) cells being infected by enterovirus 71 (EV71) and coxsackievirus B3 (CVB3), the ucMSC-EXO enhanced the expression of interferon-stimulated gene 15 (ISG15) and ISG56 to inhibit enteroviral replication, whereafter reducing the virus-induced proinflammatory factor production. This study provides a promising therapeutic strategy for ucMSC-EXO in anti-oxidative stress and antiviral effects, which provides insight into extending the function of ucMSC-EXO in cell-free therapy. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Graphical abstract

17 pages, 5874 KiB  
Article
BMS-265246, a Cyclin-Dependent Kinase Inhibitor, Inhibits the Infection of Herpes Simplex Virus Type 1
by Lefang Jiang, Yang Yu, Zhuogang Li, Yarou Gao, Haonan Zhang, Mingxin Zhang, Weihua Cao, Qun Peng and Xulin Chen
Viruses 2023, 15(8), 1642; https://doi.org/10.3390/v15081642 - 28 Jul 2023
Cited by 2 | Viewed by 1627
Abstract
Herpes simplex virus type 1 (HSV-1) infections are prevalent illnesses that can cause mucocutaneous ulcerative disease, keratitis, and genital herpes. In patients with compromised immune systems, the infection can lead to serious problems, such as encephalitis. Additionally, neonatal infections can cause brain problems [...] Read more.
Herpes simplex virus type 1 (HSV-1) infections are prevalent illnesses that can cause mucocutaneous ulcerative disease, keratitis, and genital herpes. In patients with compromised immune systems, the infection can lead to serious problems, such as encephalitis. Additionally, neonatal infections can cause brain problems and even death. Current first-line antiviral drugs are nucleoside analog inhibitors that target viral polymerase, and resistant strains have emerged. As a result, new drugs with distinct action modes are needed. Recent research indicates that cyclin-dependent kinases (CDKs) are prospective antiviral targets. Thus, CDK inhibitors may be effective antiviral agents against HSV-1 infection. In this study, we examined a panel of CDK inhibitors that target CDKs in the present study. BMS-265246 (BMS), a CDK 1/2 inhibitor, was found to effectively limit HSV-1 multiplication in Vero, HepG2, and Hela cells. A mechanism of action study suggested that BMS inhibits the early stages of viral replication when added early in the viral infection. The suppression of multiple steps in viral replication by BMS was revealed when HSV-1 infected cells were treated at different time periods in the viral life cycle. Our results suggest that BMS is a potent anti-HSV-1 agent and unique in that it may interfere with multiple steps in HSV-1 replication. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

13 pages, 2018 KiB  
Article
A Pseudovirus-Based Entry Assay to Evaluate Neutralizing Activity against Respiratory Syncytial Virus
by Longbo Hu, Jiajing Jiang, Yongjie Tang, Lingling Mei, Liping Wu, Leyi Li, Hongzhou Chen, Fei Long, Jing Xiao and Tao Peng
Viruses 2023, 15(7), 1548; https://doi.org/10.3390/v15071548 - 14 Jul 2023
Cited by 1 | Viewed by 1973
Abstract
Respiratory syncytial virus (RSV) infection can cause life-threatening pneumonia and bronchiolitis, posing a significant threat to human health worldwide, especially to children and the elderly. Currently, there is no specific treatment for RSV infection. The most effective measures for preventing RSV infection are [...] Read more.
Respiratory syncytial virus (RSV) infection can cause life-threatening pneumonia and bronchiolitis, posing a significant threat to human health worldwide, especially to children and the elderly. Currently, there is no specific treatment for RSV infection. The most effective measures for preventing RSV infection are vaccines and prophylactic medications. However, not all population groups are eligible for the approved vaccines or antibody-based preventive medications. Therefore, there is an urgent need to develop novel vaccines and prophylactic drugs available for people of all ages. High-throughput assays that evaluate the efficacy of viral entry inhibitors or vaccine-induced neutralizing antibodies in blocking RSV entry are crucial for evaluating vaccine and prophylactic drug candidates. We developed an efficient entry assay using a lentiviral pseudovirus carrying the fusion (F) protein of type A or B RSV. In addition, the essential parameters were systematically optimized, including the number of transfected plasmids, storage conditions of the pseudovirus, cell types, cell numbers, virus inoculum, and time point of detection. Furthermore, the convalescent sera exhibited comparable inhibitory activity in this assay as in the authentic RSV virus neutralization assay. We established a robust pseudovirus-based entry assay for RSV, which holds excellent promise for studying entry mechanisms, evaluating viral entry inhibitors, and assessing vaccine-elicited neutralizing antibodies against RSV. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

10 pages, 2418 KiB  
Article
β-Glucan Induces Training Immunity to Promote Antiviral Activity by Activating TBK1
by Guolei Wang, Zhiqiang Li, Mingfu Tian, Xianghua Cui, Jun’e Ma, Siyu Liu, Chenglin Ye, Li Yuan, Muhammad Suhaib Qudus, Uzair Afaq, Kailang Wu, Xinghui Liu and Chengliang Zhu
Viruses 2023, 15(5), 1204; https://doi.org/10.3390/v15051204 - 19 May 2023
Cited by 2 | Viewed by 2258
Abstract
Many studies have shown that β-glucan induces a trained immune phenotype in innate immune cells to defend against bacterial and fungal infections. The specific mechanism involves cellular metabolism and epigenetic reprogramming. However, it is unclear whether β-glucan plays a role in antiviral infection. [...] Read more.
Many studies have shown that β-glucan induces a trained immune phenotype in innate immune cells to defend against bacterial and fungal infections. The specific mechanism involves cellular metabolism and epigenetic reprogramming. However, it is unclear whether β-glucan plays a role in antiviral infection. Therefore, this study investigated the role of trained immunity induced by Candida albicans and β-glucan in antiviral innate immunity. It showed that C. albicans and β-glucan promoted the expression of interferon-β (IFN-β) and interleukin-6 (IL-6) in mouse macrophages triggered by viral infection. In addition, β-glucan pretreatment attenuated the pathological damage induced by the virus in mouse lungs and promoted the expression of IFN-β. Mechanistically, β-glucan could promote the phosphorylation and ubiquitination of TANK Binding Kinase 1 (TBK1), a key protein of the innate immune pathway. These results suggest that β-glucan can promote innate antiviral immunity, and this bioactive material may be a potential therapeutic target for antiviral treatment. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

15 pages, 2546 KiB  
Article
The SUMOylation of Human Cytomegalovirus Capsid Assembly Protein Precursor (UL80.5) Affects Its Interaction with Major Capsid Protein (UL86) and Viral Replication
by Zhigang Zhang, Sisi Xia, Zhigang Wang, Nina Yin, Jun Chen and Luyao Shao
Viruses 2023, 15(4), 931; https://doi.org/10.3390/v15040931 - 07 Apr 2023
Cited by 3 | Viewed by 1465
Abstract
Human Cytomegalovirus Capsid Assembly Protein Precursor (pAP, UL80.5) plays a key role in capsid assembly by forming an internal protein scaffold with Major Capsid Protein (MCP, UL86) and other capsid subunits. In this study, we revealed UL80.5 as a novel SUMOylated viral protein. [...] Read more.
Human Cytomegalovirus Capsid Assembly Protein Precursor (pAP, UL80.5) plays a key role in capsid assembly by forming an internal protein scaffold with Major Capsid Protein (MCP, UL86) and other capsid subunits. In this study, we revealed UL80.5 as a novel SUMOylated viral protein. We confirmed that UL80.5 interacted with the SUMO E2 ligase UBC9 (58-93aa) and could be covalently modified by SUMO1/SUMO2/SUMO3 proteins. 371Lysine located within a ψKxE consensus motif on UL80.5 carboxy-terminal was the major SUMOylation site. Interestingly, the SUMOylation of UL80.5 restrained its interaction with UL86 but had no effects on translocating UL86 into the nucleus. Furthermore, we showed that the removal of the 371lysine SUMOylation site of UL80.5 inhibited viral replication. In conclusion, our data demonstrates that SUMOylation plays an important role in regulating UL80.5 functions and viral replication. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

Review

Jump to: Editorial, Research, Other

17 pages, 1052 KiB  
Review
Prospects of Cytomegalovirus-Specific T-Cell Receptors in Clinical Diagnosis and Therapy
by Xuejie Li, Hanying Liang and Jun Fan
Viruses 2023, 15(6), 1334; https://doi.org/10.3390/v15061334 - 07 Jun 2023
Viewed by 1494
Abstract
Human cytomegalovirus (HCMV) is responsible for widespread infections worldwide. In immunocompetent individuals it is typically latent, while infection or reactivation in immunocompromised individuals can result in severe clinical symptoms or even death. Although there has been significant progress in the treatment and diagnosis [...] Read more.
Human cytomegalovirus (HCMV) is responsible for widespread infections worldwide. In immunocompetent individuals it is typically latent, while infection or reactivation in immunocompromised individuals can result in severe clinical symptoms or even death. Although there has been significant progress in the treatment and diagnosis of HCMV infection in recent years, numerous shortcomings and developmental limitations persist. There is an urgent need to develop innovative, safe, and effective treatments, as well as to explore early and timely diagnostic strategies for HCMV infection. Cell-mediated immune responses are the primary factor controlling HCMV infection and replication, but the protective role of humoral immune responses remains controversial. T-cells, key effector cells of the cellular immune system, are critical for clearing and preventing HCMV infection. The T-cell receptor (TCR) lies at the heart of T-cell immune responses, and its diversity enables the immune system to differentiate between self and non-self. Given the significant influence of cellular immunity on human health and the indispensable role of the TCR in T-cell immune responses, we posit that the impact of TCR on the development of novel diagnostic and prognostic methods, as well as on patient monitoring and management of clinical HCMV infection, will be far-reaching and profound. High-throughput and single-cell sequencing technologies have facilitated unprecedented quantitative detection of TCR diversity. With these current sequencing technologies, researchers have already obtained a vast number of TCR sequences. It is plausible that in the near future studies on TCR repertoires will be instrumental in assessing vaccine efficacy, immunotherapeutic strategies, and the early diagnosis of HCMV infection. Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Show Figures

Figure 1

Other

5 pages, 195 KiB  
Obituary
A Tribute to Professor Jianguo Wu
by Xin Chen
Viruses 2023, 15(8), 1720; https://doi.org/10.3390/v15081720 - 11 Aug 2023
Viewed by 728
Abstract
It has been a couple of months since Professor Jianguo Wu left us [...] Full article
(This article belongs to the Special Issue In Memory of Jianguo Wu)
Back to TopTop