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Molecular Research on Human Retrovirus Infection: 2nd Edition
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Molecular Research on Human Retrovirus Infection: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 3743

Special Issue Editors

Prof. Dr. Yosuke Maeda

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Guest Editor
Department of Nursing, Kibi International University, Takahashi 716-8508, Japan
Interests: HIV; HTLV-1; HERV; tuberculosis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Toshio Hattori

E-Mail Website
Guest Editor
Visiting Professor, Graduate School of Public Health, Shizuoka Graduate University of Public Health, Shizuoka 420-0881, Japan
Interests: dengue; malaria; leptospirosis; HIV; tuberculosis; inflammation; galectins; osteopontin
Special Issues, Collections and Topics in MDPI journals
Dr. Kotaro Shirakawa

E-Mail Website
Guest Editor
Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan
Interests: HIV; AIDS; APOBEC deaminase; myeloma; lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Progress has been made in preventing and treating diseases caused by human retroviruses. However, more than 40 years after discovering these viruses, there are still no vaccines or complete cures for human retrovirus infection. Human T-cell leukemia virus type 1 (HTLV-1) induces adult T-cell leukemia (ATL), and human immunodeficiency virus type 1 (HIV-1) induces acquired immune deficiency syndrome (AIDS). Both viruses infect CD4 T-cells, and HTLV-1 immortalizes and HIV kills CD4 T-cells. In this Special Issue, we welcome research reports on not only the molecular mechanisms of ATL and AIDS, but also other retrovirus-associated diseases and related opportunistic infectious diseases, including tuberculosis. Papers that propose new treatments are also welcome.

Prof. Dr. Yosuke Maeda
Prof. Dr. Toshio Hattori
Dr. Kotaro Shirakawa
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • retrovirus
  • ATL
  • HIV-1
  • AIDS

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Related Special Issue

Published Papers (3 papers)

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Research

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17 pages, 1448 KiB  
Article
No Association Between HIV-1 Subtype and Primary Resistance Mutations with CD4 Reconstitution During Effective Antiretroviral Treatment: An Observational, Cohort Study
by Andrzej Załęski, Agnieszka Lembas, Tomasz Dyda, Joanna Osińska, Joanna Jabłońska, Justyna Stempkowska-Rejek, Justyna Orzechowska and Alicja Wiercińska-Drapało
Int. J. Mol. Sci. 2025, 26(4), 1410; https://doi.org/10.3390/ijms26041410 - 7 Feb 2025
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Abstract
Some people with Human Immunodeficiency Virus (HIV) on effective antiretroviral therapy have persistent low lymphocyte CD4 counts and remain at an increased risk of Acquired Immunodeficiency Syndrome (AIDS). We investigated whether primary drug resistance mutations (DRMs) and HIV-1 subtype could be related to [...] Read more.
Some people with Human Immunodeficiency Virus (HIV) on effective antiretroviral therapy have persistent low lymphocyte CD4 counts and remain at an increased risk of Acquired Immunodeficiency Syndrome (AIDS). We investigated whether primary drug resistance mutations (DRMs) and HIV-1 subtype could be related to immunologic reconstitution in these people. In a multicenter, observational cohort study among treatment-naïve patients, we analyzed HIV-1 subtype, primary drug resistance mutations, CD4 counts, and CD4:CD8 ratios during effective antiretroviral therapy. We compared these variables between patients with different HIV subtypes and between those with or without drug-resistance mutations up to 48 weeks post-baseline. In 156 patients, CD4 count normalization (≥500 cells/µL) was observed in 39% of patients, while CD4:CD8 ratio ≥ 1 in 27% after treatment implementation. HIV-1 subtype B was present in 75% of the patients and subtype A in 22%. Primary resistance mutations were found in 57% of the individuals. The percentage of immunological nonrespondents did not differ significantly between those with different HIV subtypes or between those with or without primary resistance mutations (p > 0.05). In conclusion, there was no significant coincidence between the HIV subtype and primary drug resistance mutations with immunological reconstitution in patients receiving effective antiretroviral therapy. Full article
(This article belongs to the Special Issue Molecular Research on Human Retrovirus Infection: 2nd Edition)
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20 pages, 7853 KiB  
Article
RTL4, a Retrovirus-Derived Gene Implicated in Autism Spectrum Disorder, Is a Microglial Gene That Responds to Noradrenaline in the Postnatal Brain
by Fumitoshi Ishino, Johbu Itoh, Ayumi Matsuzawa, Masahito Irie, Toru Suzuki, Yuichi Hiraoka, Masanobu Yoshikawa and Tomoko Kaneko-Ishino
Int. J. Mol. Sci. 2024, 25(24), 13738; https://doi.org/10.3390/ijms252413738 - 23 Dec 2024
Cited by 1 | Viewed by 1258
Abstract
Retrotransposon Gag-like 4 (RTL4), a gene acquired from a retrovirus, is a causative gene in autism spectrum disorder. Its knockout mice exhibit increased impulsivity, impaired short-term spatial memory, failure to adapt to novel environments, and delayed noradrenaline (NA) recovery in the [...] Read more.
Retrotransposon Gag-like 4 (RTL4), a gene acquired from a retrovirus, is a causative gene in autism spectrum disorder. Its knockout mice exhibit increased impulsivity, impaired short-term spatial memory, failure to adapt to novel environments, and delayed noradrenaline (NA) recovery in the frontal cortex. However, due to its very low expression in the brain, it remains unknown which brain cells express RTL4 and its dynamics in relation to NA. We addressed these issues using knock-in mice carrying endogenous Rtl4 fused to Venus, which encodes a fluorescent protein. The RTL4-Venus fusion protein was detected as a secreted protein in the midbrain, hypothalamus, hippocampus and amygdala in the postnatal brain. Its signal intensity was high during critical periods of neonatal adaptation to novel environments. It was upregulated by various stimuli, including isoproterenol administration, whereas it was decreased by anesthesia but was maintained by milnacipran administration, suggesting its highly sensitive response to stressors, possible dependence on the arousal state and involvement in the NA reuptake process. In vitro mixed glial culture experiments demonstrated that Rtl4 is a microglial gene and suggested that RTL4 secretion responds rapidly to isoproterenol. Microglial RTL4 plays an important role in the NA response and possibly in the development of the NAergic neuronal network in the brain. Full article
(This article belongs to the Special Issue Molecular Research on Human Retrovirus Infection: 2nd Edition)
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Review

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30 pages, 2827 KiB  
Review
APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction
by Sharee Leong, Hesham Nasser and Terumasa Ikeda
Int. J. Mol. Sci. 2025, 26(4), 1561; https://doi.org/10.3390/ijms26041561 - 12 Feb 2025
Viewed by 1112
Abstract
The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3/A3) family of cytosine deaminases serves as a key innate immune barrier against invading retroviruses and endogenous retroelements. The A3 family’s restriction activity against these parasites primarily arises from their ability to catalyze cytosine-to-uracil [...] Read more.
The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3 (APOBEC3/A3) family of cytosine deaminases serves as a key innate immune barrier against invading retroviruses and endogenous retroelements. The A3 family’s restriction activity against these parasites primarily arises from their ability to catalyze cytosine-to-uracil conversions, resulting in genome editing and the accumulation of lethal mutations in viral genomes. Additionally, non-editing mechanisms, including deaminase-independent pathways, such as blocking viral reverse transcription, have been proposed as antiviral strategies employed by A3 family proteins. Although viral factors can influence infection progression, the determinants that govern A3-mediated restriction are critical in shaping retroviral infection outcomes. This review examines the interactions between retroviruses, specifically human immunodeficiency virus type 1 and human T-cell leukemia virus type 1, and A3 proteins to better understand how editing and non-editing activities contribute to the trajectory of these retroviral infections. Full article
(This article belongs to the Special Issue Molecular Research on Human Retrovirus Infection: 2nd Edition)
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