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This article is from Virology Journal , volume 10 . Abstract Transforming viruses can change a normal cell into a cancer cell during their normal life cycle. Persistent infections with these viruses have been recognized to cause some types of cancer. These viruses have been implicated in the modulation of various biological processes, such as proliferation, differentiation and apoptosis. The study of infections caused by oncogenic viruses had helped in our understanding of several mechanisms that regulate cell growth, as well as the molecular alterations leading to cancer. Therefore, transforming viruses provide models of study that have enabled the advances in cancer research. Viruses with transforming abilities, include different members of the Human Papillomavirus (HPV) family, Hepatitis C virus (HCV), Human T-cell Leukemia virus (HTLV-1), Epstein Barr virus (EBV) and Kaposi’s Sarcoma Herpesvirus (KSHV).Apoptosis, or programmed cell death, is a tightly regulated process that plays an important role in development and homeostasis. Additionally, it functions as an antiviral defense mechanism. The deregulation of apoptosis has been implicated in the etiology of diverse diseases, including cancer. Oncogenic viruses employ different mechanisms to inhibit the apoptotic process, allowing the propagation of infected and damaged cells. During this process, some viral proteins are able to evade the immune system, while others can directly interact with the caspases involved in apoptotic signaling. In some instances, viral proteins can also promote apoptosis, which may be necessary for an accurate regulation of the initial stages of infection.

This article is from Frontiers in Immunology , volume 5 . Abstract Human oncogenic viruses include Epstein–Barr virus, hepatitis B virus, hepatitis C virus, human papilloma virus, human T-cell lymphotropic virus, Kaposi’s associated sarcoma virus, and Merkel cell polyomavirus. It would be expected that during virus–host interaction, the immune system would recognize these pathogens and eliminate them. However, through evolution, these viruses have developed a number of strategies to avoid such an outcome and successfully establish chronic infections. The persistent nature of the infection caused by these viruses is associated with their oncogenic potential. In this article, we will review the latest information on the interaction between oncogenic viruses and the innate immune system of the host. In particular, we will summarize the available knowledge on the recognition by host pattern-recognition receptors of pathogen-associated molecular patterns present in the incoming viral particle or generated during the virus’ life cycle. We will also review the data on the recognition of cell-derived danger associated molecular patterns generated during the virus infection that may impact the outcome of the host–pathogen interaction and the development cancer.

This article is from Infectious Agents and Cancer , volume 9 . Abstract Background: Environmental factors may play a role in colon cancer. In this view, several studies investigated tumor samples for the presence of various viral DNA with conflicting results. Findings: We undertook a systematic DNA analysis of 44 consecutive, prospectively collected primary tumor samples by real time and qualitative PCR for viruses of known or potential oncogenic role in humans, including polyomavirus (JCV, BKV, Merkel cell polyomavirus), HPV, HTLV, HHV-8 and EBV. Negative controls consisted of surgical resection margins. No evidence of genomic DNA fragments from tested virus were detected, except for EBV, which was found in a significant portion of tumors (23/44, 52%). Real-time PCR showed that EBV DNA was present at a highly variable content (median 258 copies in 105 cells, range 15–4837). Presence of EBV DNA had a trend to be associated with high lymphocyte infiltration (p = 0.06, χ2 test), and in situ hybridization with EBER1-2 probes revealed latency in a fraction of these lymphoid cells, with just a few scattered plasma cells positive for BZLF-1, an immediate early protein expressed during lytic replication. LMP-1 expression was undetectable by immunohistochemistry. Conclusions: These results argue against a significant involvement of the tested oncogenic viruses in established colon cancer.

This article is from Infectious Agents and Cancer , volume 9 . Abstract Background: Environmental factors may play a role in colon cancer. In this view, several studies investigated tumor samples for the presence of various viral DNA with conflicting results. Findings: We undertook a systematic DNA analysis of 44 consecutive, prospectively collected primary tumor samples by real time and qualitative PCR for viruses of known or potential oncogenic role in humans, including polyomavirus (JCV, BKV, Merkel cell polyomavirus), HPV, HTLV, HHV-8 and EBV. Negative controls consisted of surgical resection margins. No evidence of genomic DNA fragments from tested virus were detected, except for EBV, which was found in a significant portion of tumors (23/44, 52%). Real-time PCR showed that EBV DNA was present at a highly variable content (median 258 copies in 105 cells, range 15–4837). Presence of EBV DNA had a trend to be associated with high lymphocyte infiltration (p = 0.06, χ2 test), and in situ hybridization with EBER1-2 probes revealed latency in a fraction of these lymphoid cells, with just a few scattered plasma cells positive for BZLF-1, an immediate early protein expressed during lytic replication. LMP-1 expression was undetectable by immunohistochemistry. Conclusions: These results argue against a significant involvement of the tested oncogenic viruses in established colon cancer.

The 2016 Nobel Prize in Physiology or Medicine was awarded to Dr. Yoshinori Ohsumi for his discoveries of mechanisms for autophagy. Autophagy is a fundamental and conserved cellular program essential for maintaining cellular homeostasis. Unlike non-selective autophagy (including mitophagy) that sorts harmful or surplus cellular contents to the lysosomes for degradation and recycling, selective autophagy is mediated by an increasing pool of receptors, such as p62, NBR1, TAX1BP1, NDP52, OPTN, BCL2L13, FUNDC1, CCDC50, TRIMs, and TOLLIP, and is generally invoked by certain stresses to specifically target functional substrates for lysosomal degradation to modulate various cellular responses [1- 4].

The 2016 Nobel Prize in Physiology or Medicine was awarded to Dr. Yoshinori Ohsumi for his discoveries of mechanisms for autophagy. Autophagy is a fundamental and conserved cellular program essential for maintaining cellular homeostasis. Unlike non-selective autophagy (including mitophagy) that sorts harmful or surplus cellular contents to the lysosomes for degradation and recycling, selective autophagy is mediated by an increasing pool of receptors, such as p62, NBR1, TAX1BP1, NDP52, OPTN, BCL2L13, FUNDC1, CCDC50, TRIMs, and TOLLIP, and is generally invoked by certain stresses to specifically target functional substrates for lysosomal degradation to modulate various cellular responses [1- 4].

This article is from Frontiers in Microbiology , volume 5 . Abstract HTLV-1 and HTLV-2 share broad similarities in their overall genetic organization and expression pattern, but they differ substantially in their pathogenic properties. This review outlines distinctive features of HTLV-1 and HTLV-2 that might provide clues to explain their distinct clinical outcomes. Differences in the kinetics of viral mRNA expression, functional properties of the regulatory and accessory proteins, and interactions with cellular factors and signal transduction pathways are discussed.

This article is from Frontiers in Microbiology , volume 5 . Abstract HTLV-1 and HTLV-2 share broad similarities in their overall genetic organization and expression pattern, but they differ substantially in their pathogenic properties. This review outlines distinctive features of HTLV-1 and HTLV-2 that might provide clues to explain their distinct clinical outcomes. Differences in the kinetics of viral mRNA expression, functional properties of the regulatory and accessory proteins, and interactions with cellular factors and signal transduction pathways are discussed.

This article is from Frontiers in Microbiology , volume 5 . Abstract HTLV-1 and HTLV-2 share broad similarities in their overall genetic organization and expression pattern, but they differ substantially in their pathogenic properties. This review outlines distinctive features of HTLV-1 and HTLV-2 that might provide clues to explain their distinct clinical outcomes. Differences in the kinetics of viral mRNA expression, functional properties of the regulatory and accessory proteins, and interactions with cellular factors and signal transduction pathways are discussed.

This article is from Infectious Agents and Cancer , volume 9 . Abstract Background: Oncoviruses such as HPV, KSHV, and EBV have been reported in patients with HIV infection and AIDS. How oncovirus-associated cancers rise in AIDS patients has not been fully established. The purpose of our study was to identify the viral agents in vulvar cancer and to assess their contribution to pathogenesis. Method: We retrospectively identified a total of 13 vulva tissue samples from HIV-1 positive and 9 vulvar samples from HIV-1 negative patients from the Botswana National Health Laboratory in Gaborone, Botswana, a Southern African country with a high incidence of HIV. We utilized PCR and IHC to identify HPV, EBV, KSHV, and JC virus in FFPE preserved tissue samples. Results: Using the GP5+/GP6+ primer set we detected several HPV types in tissue samples. EBV was detected in all of the positive cases (100%) and in most of the negative cases (89%). KSHV was detected in 39% of the HIV-1 positive samples and in 11% of the negative samples, and no JC virus was detected in any of the samples.Using IHC we demonstrated that LANA was expressed in 61% of the positive samples and in 44% of the negative samples. The ubiquitous EBV was more consistently expressed in negative cases (100%) than in positive cases (69%). Interestingly, the HPV-16 E6 transcript was detected in 56% of the negative samples compared to 31% of the positive samples. However, the cell cycle protein P21 used as a surrogate marker for HPV was detected in 77% of the positive samples and in 44% of the negative samples, while VEGF signals were similar in both positive (92%) and negative samples (89%). Conclusion: Our study, suggests that in Botswana, vulvar squamous cell carcinoma (VSCC) is associated with oncogenic viruses present in the niche but the contribution and progression may be regulated by HPV and other immunosuppressive infections that include HIV-1.

Six chemicals were tested for synergism in promoting in vitro oncogenic transformation of Swiss mouse 3T3 cells by herpes simplex type 2 virus (HSV-2). The test chemicals were N,Nitrosodimethylamine, 1,2-dimethylhydrazine, hydrazine, methylhydrazine, 1,1-dimethylhydrazine, and N-phenyl-alpha- naphthylamine. 1,2-dimethylhydrazine (symmetrical dimethylhydrazine, SDMH) enhanced the level of oncogenic transformation approximately two-fold. None of the other test chemicals enhanced HSV-2 transformation at the concentrations tested. The significance of these data is somewhat uncertain at this point, but certainly follow-up studies should be conducted to confirm the apparent enhancement of viral transformation by SDMH.

The objectives of this research were to develop rapid in-vitro assays, to evaluate the carcinogenic potential of chemicals used by the U.S. Air Force. Snyder-Theilen Feline Sarcoma Virus (ST-FeSV), quantitatively transforms human skin fibroblasts following second order kinetics. These studies were performed in order to determine whether chemicals altered ST-FeSV transformation in a predictable manner and to correlate the alteration with the carcinogenic or non-carcinogenic activity of the test chemical. The results, to date, show diverse carcinogens classed as: aromatic amines, polycyclic hydrocarbons, aminofluorenes, hydrazines, asbestos and mycotoxins inhibited virus transformation when virus infected cells (2 hours post-infection) were exposed to test chemical, while non-carcinogenic chemicals had no significant effect on transformation. Triton X-100, acetone, petroleum and shale oil derived JP5; RJ5 and diesel fuel, marine, demonstrated non-carcinogenic activity while formalin demonstrated carcinogenic activity. Experiments designed to show the specificity of the antagonistic effect of known carcinogens are reported.

This article is from Frontiers in Cellular and Infection Microbiology , volume 3 . Abstract A rise in technologies for epigenetic reprogramming of cells to pluripotency, highlights the potential of understanding and manipulating cellular plasticity in unprecedented ways. Increasing evidence points to shared mechanisms between cellular reprogramming and the carcinogenic process, with the emerging possibility to harness these parallels in future therapeutics. In this review, we present a synopsis of recent work from oncogenic viruses which contributes to this body of knowledge, establishing a nexus between infection, cancer, and stemness.

The objectives of this research are to develop rapid in-vitro assays to evaluate the carcinogenic potential of chemicals used by the U.S. Air Force. Snyder-Theilen Feline Sarcoma Virus (ST FeSV), quantitatively transforms human skin fibroblasts following second order kinetics. These studies were performed in order to determine whether chemicals altered ST FeSV transformation in a predictable manner and to correlate the alteration with the carcinogenic or non-carcinogenic activity of the text chemical. The results, to date, show diverse carcinogens classed as: aromatic amines, polycyclic hydrocarbons, Aminofluorenes, hydrazines, asbestos and mycotoxins inhibited virus transformation when virus infected cells (2 hours post-infection) were exposed to test chemical, while non-carcinogenic chemicals had no significant effect on transformation. Triton X-100, acetone, petroleum and shale oil derived JP5; RJ5 and diesel fuel, marine, demonstrated non-carcinogenic activity while formaline demonstrated carcinogenic activity. Experiments designed to show the specificity of the antagonistic effect of known carcinogens are reported. Disulfuram inhibits biotransformation of 1,2 symmetrical dimethyl hydrazine (SDMH) metabolites, azomethane to azoxymethane (ultimate carcinogen) thereby preventing carcinogenic effect of the proximate carcinogen SDMH. Detailed methodology required to ascertain effect of chemicals on ST FeSV pro-virus integration and synthesis are presented.

The objective of this research are to develop rapid in-vitro assays to evaluate the carcinogenic potential of chemicals used by the U.S. Air Force. Snyder-Theilen Feline Sarcoma Virus (ST FeSV), quantitatively transforms human skin fibroblasts following second order kinetics. These studies were performed in order to determine whether chemicals altered ST FeSV transformation in a predictable manner and to correlate the alteration with the carcinogenic or non-carcinogenic activity of the text chemical. The results, to date, show diverse carcinogens classed as: aromatic amines, polycyclic hydrocarbons, Aminofluorenes, hydrazines, asbestos and mycotoxins inhibited virus transformation when virus infected cells (2 hours post-infection) were exposed to test chemical, while non-carcinogenic chemicals had no significant effect on transformation. Triton X-100, acetone, petroleum and shale oil derived JP5; RJ5 and diesel fuel, marine, demonstrated non-carcinogenic activity while formaline demonstrated carcinogenic activity. Experiments designed to show the specificity of the antagonistic effect of known carcinogens are reported.