Abstract
Autophagy is an intracellular degradation pathway for long-lived proteins and organelles. This process is activated above basal levels upon cell intrinsic or environmental stress and dysregulation of autophagy has been linked to various human diseases, including those caused by viral infection. Many viruses have evolved strategies to directly interfere with autophagy, presumably to facilitate their replication or to escape immune detection. However, in some cases, modulation of autophagy appears to be a consequence of the virus disturbing the cell’s metabolic signaling networks. Here, we summarize recent advances in research at the interface of autophagy and viral infection, paying special attention to strategies that human tumor viruses have evolved.
Highlights
Hepatitis B (HBV) and C (HCV) viruses have been linked to hepatocellular carcinoma (HCC) [4], human papillomaviruses (HPVs) to cervical, anal, vulvar, vaginal, penile and oropharyngeal cancers as well as to squamous cell skin carcinomas in immunosuppressed patients [5], and the human T-lymphotropic virus 1 (HTLV-1) has been linked to adult T-cell leukemia (ATL) [6]
It is interesting to note that several viral proteins including the Epstein–Barr Virus (EBV) latent membrane protein 1 (LMP1) [13,14,15], Kaposi’s sarcoma-associated herpesvirus (KSHV) ORF49 [85], Hepatitis C virus (HCV) core and non-structural protein 3 (NS3), and HTLV-1 Tax [69] can activate the JNK signaling pathway, and this is predicted to activate Beclin-1 dependent autophagy
The ERK pathway represents the prototypical example of a mitogen-activated protein kinase (MAPK) cascade where ERK is activated by MEK, a MAPK kinase (MAPKK), which in turn is activated by RAF, a MAPKK kinase (MAPKKK)
Summary
Viruses are intracellular parasites that strictly depend on a host to replicate. after entry, they reprogram their host cells to meet their needs. Cells 2012, 1 cancers are associated with viral infections [1] Despite this substantial number, the list of human viruses that are clearly involved in the etiology of human tumors is rather short [2]. Human tumor viruses comprise a diverse group of viruses (Table 1), most of them share the ability to establish long-term latent or persistent infections In this state, the viral genome is maintained as an episomal element or as an integrated genome copy within a host chromosome, and is replicated along with the host cellular genome by the host’s DNA replication machinery. ERK, JNK and p38 modulate or have been suggested to modulate autophagy via pathways other than NF-kB, and the predictions listed in this table are based on these mechanisms [102,103,104]
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