B and T Cells in HIV and Other Viral Infections

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Infection Biology".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 969

Special Issue Editor


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Guest Editor
Department of Health Informatics, Niigata University of Health and Welfare, Niigata, Japan
Interests: human immunodeficiency virus; anti-viral immunity; vaccines; gene therapy

Special Issue Information

Dear Colleagues,

The induction of effective adaptive immune responses and the establishment of immune memory are critical for combating viral infections. So far, worldwide efforts to develop vaccines that can elicit antiviral antibody responses against viruses, including measles virus, rubella virus, varicella zoster virus, poliovirus, hepatitis B virus, influenza virus, and SARS-CoV-2, have been successful. Notably, the recent COVID-19 pandemic provided us with a large volume of data that enabled us to better understand the dynamics of B cells in response to viral infection.

On the other hand, the difficulty associated with inducing broadly neutralizing antibodies against HIV-1 due to Env's structural and highly mutable nature is an obstacle to developing an HIV-1 vaccine. HIV-1 infects and destroys helper CD4 T cells that should otherwise induce effective B-cell and antibody responses. Furthermore, HIV infection causes the alteration of B-cell populations, leading to the numerical and functional impairment of those cells. The other indispensable effector against viral infection is cellular immunity. Functional virus-specific cytotoxic T-cell responses are important to control HIV and other viral infections. However, the vaccine induction of effective CD8+ T-cell responses against HIV and simian immunodeficiency virus (SIV) remains a challenge.

In chronic viral infection, prolonged viral replication can lead to chronic immune activation and inflammation that mediate pathological conditions such as atherosclerosis and cardiovascular diseases, which can be summarized as accelerated aging. In such a case, anti-inflammatory treatment could aid in the control of disease symptoms and improve life expectancy.

This Special Issue welcomes the submission of manuscripts that describe the biological interactions between viruses and the host’s adaptive immunity. These host species are not limited to homo sapiens but include other mammalian species such as monkeys, rats, mice, chickens, and so forth, regardless of whether they are used as models of human diseases. We look forward to receiving your submissions.

Dr. Tetsuo Tsukamoto
Guest Editor

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Keywords

  • B cells
  • T cells
  • adaptive immunity
  • humoral immunity
  • cellular immunity
  • mucosal immunity
  • anti-viral immunity
  • broadly neutralizing antibodies
  • vaccine
  • immunological memory

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Published Papers (1 paper)

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Research

18 pages, 6477 KiB  
Article
A New Chimeric Antibody against the HIV-1 Fusion Inhibitory Peptide MT-C34 with a High Affinity and Fc-Mediated Cellular Cytotoxicity
by Svetlana V. Kalinichenko, Lama Ramadan, Natalia A. Kruglova, Konstantin I. Balagurov, Marina I. Lukashina, Dmitriy V. Mazurov and Mikhail V. Shepelev
Biology 2024, 13(9), 675; https://doi.org/10.3390/biology13090675 - 29 Aug 2024
Viewed by 711
Abstract
Peptides from heptad repeat (HR1 and HR2) regions of gp41 are effective inhibitors of HIV-1 entry that block the fusion of viral and cellular membranes, but the generation of antibodies highly specific for these peptides is challenging. We have previously described a mouse [...] Read more.
Peptides from heptad repeat (HR1 and HR2) regions of gp41 are effective inhibitors of HIV-1 entry that block the fusion of viral and cellular membranes, but the generation of antibodies highly specific for these peptides is challenging. We have previously described a mouse hybridoma that recognizes MT-C34-related peptides derived from HR2. It was used for the selection of HIV-1-resistant CD4 lymphocytes engineered to express the MT-C34 peptide via a CRISPR/Cas9-mediated knock-in into the CXCR4 locus. In this study, we cloned variable domains of this antibody and generated a recombinant chimeric antibody (chAb) by combining it with the constant regions of the humanized antibody Trastuzumab. The new chAb displayed a high specificity and two-fold higher level of affinity than the parental mouse monoclonal antibody. In addition, chAb mediated up to 27–43% of the antibody-dependent cellular cytotoxicity towards cells expressing MT-C34 on their surface. The anti-MT-C34 chAb can be easily generated using plasmids available for the research community and can serve as a valuable tool for the detection, purification, and even subsequent elimination of HIV-1-resistant CD4 cells or CAR cells engineered to fight HIV-1 infection. Full article
(This article belongs to the Special Issue B and T Cells in HIV and Other Viral Infections)
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