gp96 Is Critical for both Human Herpesvirus 6A (HHV-6A) and HHV-6B Infections

Ma, Jingjing; Jia, Junli; Jiang, Xuefeng; Xu, Mengyuan; Guo, Jianrong; Tang, Tian; Xu, Xianyi; Wu, Zhisheng; Hu, Benshun; Yao, Kun; Li, Lingyun; Tang, Huiping

doi:10.1128/jvi.00311-20

Cited by 9 publications

(7 citation statements)

References 55 publications

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“…They also found that HHV-6A infection promotes GRP94 expression at the cell surface. Ma et al ( 96 ) found that the viral glycoprotein gQ1 from both HHV-6A and HHV-6B interacts with GRP94 and that depletion of GRP94, competition with soluble GRP94, or its blockade with an antibody inhibited HHV-6 infection. They also found that cell surface expression of GRP94 was induced as early as 5 min postinfection.…”

Section: Glucose-regulated Proteins Grp78 and Grp94 In Viral Infectionmentioning

confidence: 99%

Endoplasmic Reticulum Chaperones in Viral Infection: Therapeutic Perspectives

Kohli

Causse

Baverel

et al. 2021

Microbiol Mol Biol Rev

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Viruses are intracellular parasites that subvert the functions of their host cells to accomplish their infection cycle. The endoplasmic reticulum (ER)-residing chaperone proteins are central for the achievement of different steps of the viral cycle, from entry and replication to assembly and exit. The most abundant ER chaperones are GRP78 (78-kDa glucose-regulated protein), GRP94 (94-kDa glucose-regulated protein), the carbohydrate or lectin-like chaperones calnexin (CNX) and calreticulin (CRT), the protein disulfide isomerases (PDIs) and the DNAJ chaperones.

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Section: Glucose-regulated Proteins Grp78 and Grp94 In Viral Infectionmentioning

confidence: 99%

Endoplasmic Reticulum Chaperones in Viral Infection: Therapeutic Perspectives

Kohli

Causse

Baverel

et al. 2021

Microbiol Mol Biol Rev

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“…Five cell lines (AV3, RD, Ht-29, VC3 and HEK293) were obtained from The European Collection of Authenticated Cell Cultures and The American Type Culture Collection. These cell lines produce the main entry factors for enteroviruses ( 45 , 46 ) and the two entry factors for HHV-6 ( 47 , 48 ). Expression of virus receptors was evaluated by indirect immunofluorescence (IF) using the primary and secondary antibodies listed in Table S1 .…”

Section: Methodsmentioning

confidence: 99%

High Prevalence of Common Human Viruses in Thyroid Tissue

et al. 2022

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IntroductionEvidence points to viral infections as possible triggers of autoimmune thyroid disease (AITD), but little is known about the prevalence of common viruses in the thyroid gland. Using a novel approach based on virus enrichment in multiple cell lines followed by detection of the viral genome and visualization of viral proteins, we investigated the presence of multiple human viruses in thyroid tissue from AITD patients and controls.MethodsThyroid tissue was collected by core needle biopsy or during thyroid surgery from 35 patients with AITD (20 Graves’ disease and 15 Hashimoto’s thyroiditis). Eighteen thyroid tissue specimens from patients undergoing neck surgery for reasons other than thyroid autoimmunity served as controls. Specimens were tested for the presence of ten different viruses. Enteroviruses and human herpesvirus 6 were enriched in cell culture before detection by PCR and immunofluorescence, while the remaining viruses were detected by PCR of biopsied tissue.ResultsForty of 53 cases (75%) carried an infectious virus. Notably, 43% of all cases had a single virus, whereas 32% were coinfected by two or more virus types. An enterovirus was found in 27/53 cases (51%), human herpesvirus 6 in 16/53 cases (30%) and parvovirus B19 in 12/53 cases (22%). Epstein-Barr virus and cytomegalovirus were found in a few cases only. Of five gastroenteric virus groups examined, only one was detected in a single specimen. Virus distribution was not statistically different between AITD cases and controls.ConclusionCommon human viruses are highly prevalent in the thyroid gland. This is the first study in which multiple viral agents have been explored in thyroid. It remains to be established whether the detected viruses represent causal agents, possible cofactors or simple bystanders.

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“…The plasmids pcDNA3.1Flag-MAVS, pcDNA3.1HA-MAVS, pcDNA3.1Myc-STING, and pcDNA3.1Flag-TBK1 were kindly provided by Jingfeng Wang (Chinese Academy of Medical Sciences). For knockdown experiments, we used a modified pLKO.1 plasmid ( 58 ). Oligonucleotide 1 was generated using the primers 5′-CCGGGCGTTTCTCCTGCCGTTTACTCGAGAGTAAACGGCAGGAGAAACGTTTTTT-3′ and 5′-AATTAAAAAACGTTTCTCCTGCCGTTTACTCTCGAGTAAACGGCAGGAGAAACGC-3′, and oligonucleotide 2 was generated using the primers 5′-CCGGGGATGGATGATACGATCATCTCGAGAGATGATCGTATCATCCATCCTTTTTT-3′ and 5′-AATTAAAAAAGGATGGATGATACGATCATCTCTCGAGATGATCGTATCATCCATCC-3′.…”

Section: Methodsmentioning

confidence: 99%

Human Herpesvirus 6B U26 Inhibits the Activation of the RLR/MAVS Signaling Pathway

Jiang

Tang

Guo

et al. 2021

mBio

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U26 is one of the roseolovirus unique genes with unknown function. Human herpesvirus 6B (HHV-6B) pU26 is predicted to be an 8-transmembrane protein containing a mitochondrion location signal. Here, we analyzed U26 function during HHV-6B infection and find that (i) HHV-6B U26 is expressed at a very early stage during HHV-6B infection, and knockdown of it results in a significant decrease of HHV-6B progeny virus production; (ii) U26 inhibits the activation of the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR)/mitochondrial antiviral signaling protein (MAVS) signaling pathway, an important anti-HHV-6B infection innate immune response, by targeting MAVS protein for degradation; and (iii) a portion of U26 locates to the mitochondria, which could affect the mitochondrial membrane potential and finally leads to MAVS degradation. These findings indicate that HHV-6B U26 is a novel antagonistic viral factor against host innate antiviral immunity. IMPORTANCE HHV-6B (human herpesvirus 6B) is well known to evade host antiviral responses and establish a lifelong latent infection. How HHV-6B evades RNA recognition is still poorly understood. Our results indicate that HHV-6 U26 plays a vital role in RLR/MAVS signaling pathway activity. Knockout of endogenous MAVS could facilitate HHV-6B replication. The findings in this study could provide new insights into host-virus interactions and help develop a new therapy against HHV-6B infection.

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gp96 Is Critical for both Human Herpesvirus 6A (HHV-6A) and HHV-6B Infections

Cited by 9 publications

References 55 publications

Endoplasmic Reticulum Chaperones in Viral Infection: Therapeutic Perspectives

Endoplasmic Reticulum Chaperones in Viral Infection: Therapeutic Perspectives

High Prevalence of Common Human Viruses in Thyroid Tissue

Human Herpesvirus 6B U26 Inhibits the Activation of the RLR/MAVS Signaling Pathway

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