scholarly journals Virus infection induced pulmonary fibrosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Jie Huang ◽  
Xiao Xiao Tang
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Pulmonary Fibrosis ◽  
Leukemia Virus ◽  
Interstitial Lung Diseases ◽  
Barr Virus ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Epstein Barr ◽  
The Relationship

AbstractPulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the relationship between virus infection and pulmonary fibrosis is getting more and more attention, especially after the outbreak of SARS-CoV-2 in 2019, however, the mechanisms underlying the virus-induced pulmonary fibrosis are not fully understood. Here, we review the relationship between pulmonary fibrosis and several viruses such as Human T-cell leukemia virus (HTLV), Human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Epstein–Barr virus (EBV), Murine γ-herpesvirus 68 (MHV-68), Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome (MERS)-CoV, Severe acute respiratory syndrome (SARS)-CoV and SARS-CoV-2 as well as the mechanisms underlying the virus infection induced pulmonary fibrosis. This may shed new light on the potential targets for anti-fibrotic therapy to treat pulmonary fibrosis induced by viruses including SARS-CoV-2.

scholarly journals Analysis of Interleukin-27 (EBI3/p28) Expression in Epstein-Barr Virus- and Human T-Cell Leukemia Virus Type 1-Associated Lymphomas

2005 ◽  
Vol 166 (4) ◽  
pp. 1217-1228 ◽  
Author(s):  
Frédérique Larousserie ◽  
Emilie Bardel ◽  
Stefan Pflanz ◽  
Bertrand Arnulf ◽  
Carmen Lome-Maldonado ◽  
...  
Keyword(s):  
T Cell ◽  
Epstein Barr Virus ◽  
Leukemia Virus ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Barr Virus ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Epstein Barr

Viruses

2016 ◽  
pp. 136-141
Author(s):  
Chris Boshoff
Keyword(s):  
Viral Infections ◽  
Leukemia Virus ◽  
Hepatocellular Cancer ◽  
Merkel Cell ◽  
Individual Level ◽  
Underdeveloped Countries ◽  
Barr Virus ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Epstein Barr

This chapter covers the relationship between viruses and cancer, which account for up to 15% of all human cancers. It discusses the aetiology of cancer regarding herpesviruses, Epstein-Barr virus (EBV), Burkitt lymphoma (BL), nasopharyngeal carcinoma (NPC), Hodgkin disease (HD), post-transplant lymphoproliferative disorder (PTLD), Kaposi’s sarcoma-associated herpesvirus (KSHV), Multicentric Castleman’s Disease (MCD), papillomaviruses (HPV), Human T-cell Leukemia virus 1 (HTLV-1), Hepatitis B virus (HBV), Hepatocellular carcinoma (HCC), Hepatitis C virus (HCV), Merkel cell polyomavirus (MCV), and Merkel cell carcinoma (MCC). Many of these are associated with viral infections are preventable, either at an individual level or societally, and are more common in immunocompromised individuals. Worldwide, particularly in underdeveloped countries, the greatest impact on global cancer health would be on the reduction or elimination of virally-associated hepatocellular cancer and cervical cancer by immunization for HBV and HPV.

scholarly journals Lymphotropic Viruses: Chronic Inflammation and Induction of Cancers

Biology ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 390
Author(s):  
Edward W. Harhaj ◽  
Noula Shembade
Keyword(s):  
Transcription Factors ◽  
Chronic Inflammation ◽  
De Novo ◽  
Leukemia Virus ◽  
Cell Leukemia Virus Type ◽  
Barr Virus ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Control Virus ◽  
Epstein Barr

Inflammation induced by transcription factors, including Signal Transducers and Activators of Transcription (STATs) and NF-κB, in response to microbial pathogenic infections and ligand dependent receptors stimulation are critical for controlling infections. However, uncontrolled inflammation induced by these transcription factors could lead to immune dysfunction, persistent infection, inflammatory related diseases and the development of cancers. Although the induction of innate immunity and inflammation in response to viral infection is important to control virus replication, its effects can be modulated by lymphotropic viruses including human T-cell leukemia virus type 1 (HTLV-1), Κaposi’s sarcoma herpesvirus (KSHV), and Epstein Barr virus (EBV) during de novo infection as well as latent infection. These lymphotropic viruses persistently activate JAK-STAT and NF-κB pathways. Long-term STAT and NF-κB activation by these viruses leads to the induction of chronic inflammation, which can support the persistence of these viruses and promote virus-mediated cancers. Here, we review how HTLV-1, KSHV and EBV hijack the function of host cell surface molecules (CSMs), which are involved in the regulation of chronic inflammation, innate and adaptive immune responses, cell death and the restoration of tissue homeostasis. Thus, better understanding of CSMs-mediated chronic activation of STATs and NF-κB pathways in lymphotropic virus-infected cells may pave the way for therapeutic intervention in malignancies caused by lymphotropic viruses.

An EBV genome carrying pre-B cell leukemia in a homosexual man with characteristic karyotype and impaired EBV-specific immunity.

1986 ◽  
Vol 4 (10) ◽  
pp. 1481-1488 ◽  
Author(s):  
I Ernberg ◽  
M Björkholm ◽  
L Zech ◽  
B Sandstedt ◽  
R Szigeti ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Leukemia Virus ◽  
Partial Trisomy ◽  
Cell Leukemia ◽  
Barr Virus ◽  
Human T Cell ◽  
Excellent Health ◽  
T Cell Leukemia Virus ◽  
Epstein Barr

A Burkitt-like lymphoma/leukemia confined to bone marrow was detected in a human T cell leukemia virus (HTLV)-III/LAV- and Epstein-Barr virus (EBV)-seropositive homosexual man. The tumor cells were EBNA-positive and contained at least 22 EBV genomes per cell. They were totally immunoglobin negative, but showed other markers for B cells detected with monoclonal antibodies. The patient had an impaired cellular immunity to EBV antigens and EBV-infected cells at diagnosis, but these reactions normalized during treatment. Cell clones derived from the bone marrow tumor in vitro also carried EBV and had six different marker chromosomes, including the typical 14q+ chromosome and a t(8 - ;8), which resulted in trisomy for the largest part of 8q. Partial trisomy for 12q was also observed. The patient completed six courses of combination chemotherapy and remains in excellent health after 34 months of follow-up.

scholarly journals Correlation between human T cell leukemia virus type 1 infection and hepatitis virus infection.

1993 ◽  
Vol 39 (6) ◽  
pp. 911-916
Author(s):  
Shizuko Yakabi ◽  
Hiroki Zukeran ◽  
Yasuhiro Miyagi ◽  
Reiko Taira ◽  
Hiroshi Sakugawa ◽  
...  
Keyword(s):  
T Cell ◽  
Virus Infection ◽  
Hepatitis Virus ◽  
Leukemia Virus ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
T Cell Leukemia Virus ◽  
Hepatitis Virus Infection

Inhibition of NF-κB induces apoptosis of KSHV-infected primary effusion lymphoma cells

Blood ◽  
2000 ◽  
Vol 96 (7) ◽  
pp. 2537-2542 ◽  
Author(s):  
Shannon A. Keller ◽  
Elaine J. Schattner ◽  
Ethel Cesarman
Keyword(s):  
Primary Effusion Lymphoma ◽  
Leukemia Virus ◽  
Human Lymphocytes ◽  
Kaposi Sarcoma ◽  
Irreversible Inhibitor ◽  
Mobility Shift ◽  
Lymphoma Cells ◽  
Barr Virus ◽  
Human T Cell ◽  
Epstein Barr

Abstract Kaposi sarcoma–associated herpesvirus (KSHV), or human herpervirus 8 (HHV-8), is a γ-herpesvirus that infects human lymphocytes and is associated with primary effusion lymphoma (PEL). Currently, the role of viral infection in the transformation of PEL cells is unknown. One possibility is that KSHV, like the lymphotropic viruses Epstein-Barr virus (EBV) and human T-cell leukemia virus I (HTLV-I), activates the transcription factor NF-κB to promote survival and proliferation of infected lymphocytes. To examine this possibility, we assessed NF-κB activity in KSHV-infected PEL cell lines and primary tumor specimens by electrophoretic mobility shift assay (EMSA). We observed that NF-κB is constitutively activated in all KSHV-infected lymphomas, and consists of 2 predominant complexes, p65/p50 heterodimers and p50/p50 homodimers. Inhibition experiments demonstrated that Bay 11-7082, an irreversible inhibitor of IκBα phosphorylation, completely and specifically abrogated the NF-κB/DNA binding in PEL cells. PEL cells treated with Bay 11 demonstrated down-regulation of the NF-κB inducible cytokine interleukin 6 (IL-6), and apoptosis. These results suggest that NF-κB activity is necessary for survival of KSHV-infected lymphoma cells, and that pharmacologic inhibition of NF-κB may be an effective treatment for PEL.

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