Reviews
- The crosstalk between bacteria and host autophagy: host defense or bacteria offense
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Lin Zheng , Fang Wei , Guolin Li
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J. Microbiol. 2022;60(5):451-460. Published online April 29, 2022
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DOI: https://doi.org/10.1007/s12275-022-2009-z
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62
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6
Web of Science
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7
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Abstract
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Xenophagy is a specific selective autophagy for the elimination
of intracellular bacteria. Current evidence suggests that the
processes for host autophagy system to recognize and eliminate
invading bacteria are complex, and vary according to
different pathogens. Although both ubiquitin-dependent and
ubiquitin-independent autophagy exist in host to defense invading
bacteria, successful pathogens have evolved diverse
strategies to escape from or paralyze host autophagy system.
In this review, we discuss the mechanisms of host autophagy
system to recognize and eliminate intracellular pathogens and
the mechanisms of different pathogens to escape from or paralyze
host autophagy system, with a particular focus on the
most extensively studied bacteria.
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Citations
Citations to this article as recorded by

- Complement C3 deposition restricts the proliferation of internalized Staphylococcus aureus by promoting autophagy
Yining Deng, Yunke Zhang, Tong Wu, Kang Niu, Xiaoyu Jiao, Wenge Ma, Chen Peng, Wenxue Wu
Frontiers in Cellular and Infection Microbiology.2024;[Epub] CrossRef - Innate immune response of host cells infected with Salmonella
Hongfei Fan, Juane Lu, Hao Wu, Haihua Ruan, Wenjun Song, Y.-T. Yu, P.P. Piccaluga, S. Xie
BIO Web of Conferences.2024; 111: 01022. CrossRef - Exploring the Connections: Autophagy, Gut Microbiota, and Inflammatory Bowel Disease Pathogenesis
Arunkumar Subramanian, Afrarahamed J, Tamilanban T, Vinoth Kumarasamy, M Yasmin Begum, Mahendran Sekar, Vetriselvan Subramaniyan, Ling Shing Wong, Adel Al Fatease
Journal of Inflammation Research.2024; Volume 17: 10453. CrossRef - Programmed cell death and Salmonella pathogenesis: an interactive overview
Yu Zhang, Maodou Xu, Yujiao Guo, Li Chen, Wanwipa Vongsangnak, Qi Xu, Lizhi Lu
Frontiers in Microbiology.2024;[Epub] CrossRef - Bacterial lipoprotein plays an important role in the macrophage autophagy and apoptosis induced by Salmonella typhimurium and Staphylococcus aureus
Shanshan Jiang, Jinyao He, Lijie Zhang, Qiaojiajie Zhao, Shuqi Zhao
Open Life Sciences.2023;[Epub] CrossRef - Xenophagy as a Strategy for Mycobacterium leprae Elimination during Type 1 or Type 2 Leprosy Reactions: A Systematic Review
Débora Dantas Nucci Cerqueira, Ana Letícia Silva Pereira, Ana Elisa Coelho da Costa, Tarcísio Joaquim de Souza, Matheus Santos de Sousa Fernandes, Fabrício Oliveira Souto, Patrícia d’Emery Alves Santos
Pathogens.2023; 12(12): 1455. CrossRef - Brucella BtpB Manipulates Apoptosis and Autophagic Flux in RAW264.7 Cells
Junmei Li, Lin Qi, Ziyang Diao, Mengyu Zhang, Bin Li, Yunyi Zhai, Mingyue Hao, Dong Zhou, Wei Liu, Yaping Jin, Aihua Wang
International Journal of Molecular Sciences.2022; 23(22): 14439. CrossRef
- [Minireview] Primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas
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Sangmin Kang , Jinjong Myoung
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J. Microbiol. 2017;55(5):319-329. Published online April 29, 2017
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DOI: https://doi.org/10.1007/s12275-017-7075-2
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55
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12
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Abstract
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Kaposi’s sarcoma-associated herpesvirus (KSHV) is the latest addition to the human herpesvirus family. Unlike alpha- and beta-herpesvirus subfamily members, gamma-herpesviruses, including Epstein-Barr virus (EBV) and KSHV, cause vari-ous tumors in humans. KSHV primarily infects endothelial and B cells in vivo, and is associated with at least three malig-nancies: Kaposi’s sarcoma and two B cell lymphomas, res-pectively. Although KSHV readily infects endothelial cells in vitro and thus its pathogenic mechanisms have been exten-sively studied, B cells had been refractory to KSHV infection. As such, functions of KSHV genes have mostly been eluci-dated in endothelial cells in the context of viral infection but not in B cells. Whether KSHV oncogenes, defined in endo-thelial cells, play the same roles in the tumorigenesis of B cells remains an open question. Only recently, through a few ground-breaking studies, B cell infection models have been established. In this review, those models will be compared and contrasted and putative mechanisms of KSHV-induced B cell transformation will be discussed.
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Citations
Citations to this article as recorded by

- Folate-Targeted Nanocarriers Co-Deliver Ganciclovir and miR-34a-5p for Combined Anti-KSHV Therapy
Fangling Li, Dongdong Cao, Wenyi Gu, Dongmei Li, Zhiyong Liu, Lin Cui
International Journal of Molecular Sciences.2024; 25(5): 2932. CrossRef - Structural aspects of hepatitis E virus
Florencia Cancela, Ofelia Noceti, Juan Arbiza, Santiago Mirazo
Archives of Virology.2022; 167(12): 2457. CrossRef - iTIME.219: An Immortalized KSHV Infected Endothelial Cell Line Inducible by a KSHV-Specific Stimulus to Transition From Latency to Lytic Replication and Infectious Virus Release
Stephen J. Dollery, Tania D. Maldonado, Eric A. Brenner, Edward A. Berger
Frontiers in Cellular and Infection Microbiology.2021;[Epub] CrossRef - Analysis of KSHV B lymphocyte lineage tropism in human tonsil reveals efficient infection of CD138+ plasma cells
Farizeh Aalam, Romina Nabiee, Jesus Ramirez Castano, Jennifer Totonchy, Vera L. Tarakanova
PLOS Pathogens.2020; 16(10): e1008968. CrossRef - Molecular Virology of KSHV in the Lymphocyte Compartment—Insights From Patient Samples and De Novo Infection Models
Farizeh Aalam, Jennifer Totonchy
Frontiers in Cellular and Infection Microbiology.2020;[Epub] CrossRef - Molecular and cellular interplay in virus-induced tumors in solid organ recipients
Alessia Gallo, Monica Miele, Ester Badami, Pier Giulio Conaldi
Cellular Immunology.2019; 343: 103770. CrossRef - Middle East respiratory syndrome coronavirus-encoded ORF8b strongly antagonizes IFN-β promoter activation: its implication for vaccine design
Jeong Yoon Lee, Sojung Bae, Jinjong Myoung
Journal of Microbiology.2019; 57(9): 803. CrossRef - Methyltransferase of a cell culture-adapted hepatitis E inhibits the MDA5 receptor signaling pathway
Jinjong Myoung, Jeong Yoon Lee, Kang Sang Min
Journal of Microbiology.2019; 57(12): 1126. CrossRef - Cell Type-Specific Interferon-γ-mediated Antagonism of KSHV Lytic Replication
Mi-Kyung Park, Hyejeong Cho, Seong Woon Roh, Seong-Jun Kim, Jinjong Myoung
Scientific Reports.2019;[Epub] CrossRef - Comment on primary lymphocyte infection models for KSHV and its putative tumorigenesis mechanisms in B cell lymphomas (Journal of Microbiology 2017, 55(5): 319-329)
Giovanna Rappocciolo, Frank Jenkins, Charles R. Rinaldo
Journal of Microbiology.2017; 55(7): 592. CrossRef - Lipids, lipid metabolism and Kaposi’s sarcoma-associated
herpesvirus pathogenesis
Lu Dai, Zhen Lin, Wei Jiang, Erik K. Flemington, Zhiqiang Qin
Virologica Sinica.2017; 32(5): 369. CrossRef - The Roles of Matricellular Proteins in Oncogenic Virus-Induced Cancers and Their Potential Utilities as Therapeutic Targets
Naoyoshi Maeda, Katsumi Maenaka
International Journal of Molecular Sciences.2017; 18(10): 2198. CrossRef
Research Support, Non-U.S. Gov't
- KSHV Infection of B-Cell Lymphoma Using a Modified KSHV BAC36 and Coculturing System
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Hyosun Cho , Hyojeung Kang
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J. Microbiol. 2012;50(2):285-292. Published online April 27, 2012
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DOI: https://doi.org/10.1007/s12275-012-1495-9
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43
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6
Scopus
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Abstract
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Kaposi’s sarcoma-associated herpesvirus (KSHV) is the
causative agent of two B cell lymphoproliferative diseases,
namely primary effusion lymphoma (PEL) and multicentric
Castleman’s disease (MCD). KSHV infection of B cell lymphoma
in vitro has been a long-standing battle in advancing
human KSHV biology. In this study, a modified form of
KSHV BAC36 named BAC36A significantly increased the
fidelity of gene-targeted site-directed mutagenesis in the
KSHV genome. This modification eliminates tedious screening
steps required to obtain mutant clones when a KSHV
BAC36 reverse genetic system is used. Coculturing B-cell
lymphoma BJAB cells with KSHV BAC36A stably transfected
293T cells enabled us to infect BJAB cells with a
KSHV virion derived from the KSHV BAC36A. The coculture
system produced substantial amounts of KSHV infection
to BJAB, meaning that KSHV virions were released
from 293T cells and then infected neighboring BJAB cells.
Owing to our success with the KSHV BAC36A and coculture
system, we propose a new genetic system for the study of
KSHV gene expression and regulation in B-cell lymphoma.