Reticuloendotheliosis virus and avian leukosis virus subgroup J synergistically increase the accumulation of exosomal miRNAs

Zhou, Defang; Xue, Jingwen; He, Shuhai; Du, Xusheng; Zhou, Jing; Li, Chengui; Huang, Libo; Nair, Venugopal; Yao, Yongxiu; Cheng, Ziqiang

doi:10.1186/s12977-018-0427-0

Cited by 26 publications

(33 citation statements)

References 45 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miR‐146a was also reported to be strongly increased in EVs isolated from cells coinfected with reticuloendotheliosis virus and avian leukosis virus subgroup J. Although a function of the secreted miRNAs was not explicitly shown in this report, bioinformatic target prediction suggests participation in virus–vector integration and energy metabolism (D. Zhou et al, ). Since miR‐146 is known to be upregulated inside infected cells, it will be of interest to understand if the increased secretion of miR‐146 involves passive or active sorting mechanisms (Box ).…”

Section: Secreted Host Mirnas Promote Viral Infection and Contribute mentioning

confidence: 80%

Extracellular RNA in viral–host interactions: Thinking outside the cell

et al. 2019

View full text Add to dashboard Cite

Small RNAs and their associated RNA interference (RNAi) pathways underpin diverse mechanisms of gene regulation and genome defense across all three kingdoms of life and are integral to virus–host interactions. In plants, fungi and many animals, an ancestral RNAi pathway exists as a host defense mechanism whereby viral double‐stranded RNA is processed to small RNAs that enable recognition and degradation of the virus. While this antiviral RNAi pathway is not generally thought to be present in mammals, other RNAi mechanisms can influence infection through both viral‐ and host‐derived small RNAs. Furthermore, a burgeoning body of data suggests that small RNAs in mammals can function in a non‐cell autonomous manner to play various roles in cell‐to‐cell communication and disease through their transport in extracellular vesicles. While vesicular small RNAs have not been proposed as an antiviral defense pathway per se, there is increasing evidence that the export of host‐ or viral‐derived RNAs from infected cells can influence various aspects of the infection process. This review discusses the current knowledge of extracellular RNA functions in viral infection and the technical challenges surrounding this field of research. This article is categorized under: Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs RNA in Disease and Development > RNA in Disease Regulatory RNAs/RNAi/Riboswitches > RNAi: Mechanisms of Action

show abstract

Section: Secreted Host Mirnas Promote Viral Infection and Contribute mentioning

confidence: 80%

Extracellular RNA in viral–host interactions: Thinking outside the cell

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Congenitally infected chickens are characterized by the presence of high levels of virus in the blood and tissues, but the absence of antivirus-specific antibodies [5–7]. In particular, immunological tolerance induced by ALV-J is an essential factor for neoplasia and opportunistic infection [8–10]. However, little is still known about the pathogenesis of immunological tolerance caused by the congenital infection of ALV-J.…”

Section: Introductionmentioning

confidence: 99%

Clonal anergy of CD117+chB6+ B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance

Zheng

Zhou

et al. 2019

Retrovirology

Self Cite

View full text Add to dashboard Cite

BackgroundThe pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown.ResultsIn this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies. In congenitally infected chickens, immune organs, particularly the bursa of Fabricius, were poorly developed. Moreover, IgM-and IgG-positive cells and total immunoglobulin levels were significantly decreased in these chickens. Large numbers of bursa follicles with no differentiation into cortex and medulla indicated that B cell development was arrested at the early stage. Flow cytometry analysis further confirmed that ALV-J blocked the differentiation of CD117+chB6+ B cell progenitors in the bursa of Fabricius. Furthermore, both the humoral immunity and the immunological capability of B cells and their progenitors were significantly suppressed, as assessed by (a) the antibody titres against sheep red blood cells and the Marek’s disease virus attenuated serotype 1 vaccine; (b) the proliferative response of B cells against thymus-independent antigen lipopolysaccharide (LPS) in the spleen germinal centres; and (c) the capacities for proliferation, differentiation and immunoglobulin gene class-switch recombination of B cell progenitors in response to LPS and interleukin-4(IL-4) in vitro.ConclusionsThese findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J.

show abstract

“…However, compared with control, there were no changes of TRIM62 mRNA levels at another time point (Figure 1B). The REV mRNA expression was upregulated and reached the plateau at 96 h post-infection in CEF cells (17).…”

Section: Rev Infection Affected Trim62 Expression In Cef Cellsmentioning

confidence: 97%

“…The CEF cells were lysed in RIPA lysis buffer [25 mM Tris (pH 7.4), 150 mM NaCl, 1 mM EDTA, 1% NP-40, 5% glycerol] containing protease and phosphatase inhibitor cocktails (Novasygen, Beijing, China). The lysis was separated by SDS-PAGE and transferred to PVDF membranes (Millipore, Bedford, USA) as reported previously (17,18). The target proteins were detected with specific primary antibodies against TRIM62 (19) and REV env (primary antibodies were prepared by our laboratory, anti-REV gp90) at a 1:200, 1:500, and 1:3,000 dilution, respectively.…”

Section: Western Blottingmentioning

confidence: 99%

TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication

Niu

Yang

et al. 2020

Front. Vet. Sci.

Self Cite

View full text Add to dashboard Cite

Emerging evidence suggests that the tripartite motif containing 62 (TRIM62), a member of the TRIM family, plays an important role in antiviral processes. The objective of the study was to explore the role of TRIM62 in reticuloendotheliosis virus (REV) infection and its potential molecular mechanism. We first demonstrated that the REV infection affected the TRIM62 expression first upregulated and then downregulated in CEF cells. Next, we evaluated the effect of TRIM62 on viral replication. Overexpression of TRIM62 decreased REV replication. On the contrary, silencing of endogenously expressed TRIM62 increased viral replication. Then, to explore the necessity of domains in TRIM62's negative regulation on viral replication, we transfected CEF cells with TRIM62 domain deletion mutants. Deletion domain partially abolished TRIM62's antiviral activity. The effect of SPRY domain deletion was the highest and that of coiled-coil was the lowest. Further, we identified 18 proteins that coimmunoprecipitated and interacted with TRIM62 by immunocoprecipitation and mass spectrometry analysis. Strikingly, among which, both Ras-related protein Rab-5b (RAB5B) and Arp2/3 complex 34-kDa subunit (ARPC2) were involved in actin cytoskeletal pathway. Altogether, these results strongly suggest that chicken TRIM62 provides host defense against viral infection, and all domains are required for its action. RAB5B and ARPC2 may play important roles in its negative regulation processes.Keywords: TRIM62, negative regulation, reticuloendotheliosis virus, domain deletion, RAB5B and ARPC2 FIGURE 2 | Restriction of REV replication in CEF cells induced by TRIM62. (A,B) CEF cells were transfected with pTRIM62 or empty vector before infection with REV. The expression levels of TRIM62 (A) and REV (B) were assessed by qRT-PCR and Western blotting. (C,D) CEF cells were transfected with shTRIM62 or a negative-control shRNA before infection with REV. The expression levels of TRIM62 (C) and REV (D) were determined by qPCR and Western blotting.

show abstract

Reticuloendotheliosis virus and avian leukosis virus subgroup J synergistically increase the accumulation of exosomal miRNAs

Cited by 26 publications

References 45 publications

Extracellular RNA in viral–host interactions: Thinking outside the cell

Extracellular RNA in viral–host interactions: Thinking outside the cell

Clonal anergy of CD117+chB6+ B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance

TRIM62 From Chicken as a Negative Regulator of Reticuloendotheliosis Virus Replication

Contact Info

Product

Resources

About