Lymphotropic Viruses: Chronic Inflammation and Induction of Cancers.
Edward William HarhajNoula ShembadePublished in: Biology (2020)
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.
Keyphrases
- oxidative stress
- epstein barr virus
- immune response
- induced apoptosis
- transcription factor
- signaling pathway
- cell death
- lps induced
- diffuse large b cell lymphoma
- nuclear factor
- endothelial cells
- randomized controlled trial
- cell cycle arrest
- cell surface
- inflammatory response
- cell proliferation
- genetic diversity
- bone marrow
- microbial community
- toll like receptor
- drug induced
- disease virus