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Antiviral Drugs as Tools for Nanomedicine
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
Cancer is an abnormal condition in which a few cells behave against the normal physiological rules and divide and grow uncontrollably. It remains a leading cause of death worldwide. Infectious agents, such as viruses, bacteria, and parasites, behave as etiological agents in ~20% of human cancers, out of which nearly 12% of cancers worldwide are caused by oncovirus. The conventional treatments individually are not effective, and therefore, combinatorial therapies were introduced to control cancer; however the side effects still remain associated with them due to their nonspecificity. Use of a nano-carrier system proves to be effective in cancer treatment due to its drug-entrapment efficiency, target specificity, and long circulation half-life. Various nano drug-delivery platforms and current research are thoroughly described further. This chapter emphasises the advancement in use of nano-delivery platforms for toxic antiviral drugs against viruses which are known to cause cancer directly or indirectly.
Viruses and Antiviral Agents
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Richard B. Townsley, Camille A. Huser, Chris Hansell
A virus that can cause cancer is called an oncovirus. In 2008, of the estimated 12.7 million new cases of cancer worldwide, 1.9 million were attributable to hepatitis B and C virus, human papilloma virus and helicobacter pylori infections.19 With regard to primary head and neck malignancies, the International Agency for Research on Cancer has identified Epstein-Barr virus and human papilloma virus as causative oncoviruses for nasopharyngeal cancer and oropharyngeal cancer respectively.20
Virus Wars
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Markus Vähä-Koskela, Fabrice Le Boeuf, Vincenzo Cerullo
Although several potential molecular and immunological oncovirus complementation mechanisms of oncolytic viruses have been presented here, the sum of oncolytic virus replication/antitumor efficacy in oncovirus-associated cancers is difficult to predict due to multiple overlapping and, in many cases, promoting and inhibitory pathways. Therefore, empirical testing remains the most viable way of establishing whether an oncolytic virus would be suitable to target a particular type of oncovirus-induced tumor. Here we provide examples of such testing, where the aim has specifically been to combat oncovirus tumors through molecular exploitation by the oncolytic virus. We also highlight some unwitting targeting of oncovirus-induced tumors (unwitting because oncovirus etiology and/or presence was not known or not addressed).
Retroviruses in the pathogenesis of systemic lupus erythematosus: Are they potential therapeutic targets?
Published in Autoimmunity, 2020
Rossella Talotta, Fabiola Atzeni, Magdalena Janina Laska
Exogenous retroviruses comprise the oncovirus HTLV and the lentivirus HIV, which are associated to lympho-proliferative and neurologic disorders and acquired immunodeficiency syndrome (AIDS), respectively [56]. Data on the association between HTLV and SLE are conflicting [30,57,58]. HTLV could induce SLE by means of molecular mimicry or acting on cluster of differentiation (CD)4+ T lymphocyte and cytokine secretion [29]. HTLV is, in fact, a complex retrovirus coding for regulatory proteins that can activate several survival and inflammatory pathways in infected immune cells, like those directed by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein 1 (AP-1). This results in the up-regulation of T helper (Th)1 lymphocyte subset at detriment of T regulatory cells, with the following unbalance in the secreted cytokines. Some reports have shown that SLE patients have variable rates of anti-HTLV antibodies that can dictate a different phenotype [57–61]. According to a study, in fact, seropositive SLE patients have a late onset of the disease and a milder course characterised by less lymphopenia and a lower dose of steroids needed [62]. However, data confirming the association between HTLV and SLE are weak: insofar, HTLV may be the initial trigger of autoimmunity through molecular mimicry between the epitopes of a 28-kDa protein coded by HTLV-related endogenous sequence-1 (HRES-1) and those of the HTLV-I gag p24 [63].
Low Epstein-Barr virus count in sinonasal inverted papilloma
Published in Acta Oto-Laryngologica, 2020
Alexandra Schindele, Anna Holm, Karin Nylander, Annika Allard, Katarina Olofsson
SIP is most likely characterized by a multi-mediator and -step aetiology with a strong tendency to recur and grow invasively despite its benign histology [4]. This strongly implicates an infectious aetiology. HPV has been suggested as a potential aetiological agent for sinonasal papillomas and their associated malignancies [13]. The role of EBV as a recognized oncovirus in the development of SIP is still unclear, and also if concurrency of HPV and EBV can enhance promotional events in a multistep oncogenesis. Our research group has previously published an HPV and p16 analysis on the same biopsy material [12], and we found no co-expression between HPV and EBV.
Ampelopsin Induces DR5-Mediated Apoptotic Cell Death in EBV-Infected Cells through the p38 Pathway
Published in Nutrition and Cancer, 2020
Sun-Mi Yun, Yeong Seok Kim, Ki Hoon Kim, Dae Young Hur
Epstein-Barr virus (EBV) is a γ-herpes virus that infects more than 90% of the individuals on Earth (1). EBV is the first oncovirus to be characterized (2), and its function is well-known in human tumors, including Burkitt’s lymphoma, non-Hodgkin’s lymphoma, nasopharyngeal carcinoma, and gastric cancer (3). The World Health Organization (WHO) estimates that there are 400,000 cases of EBV-related cancer each year (4). EBV encodes a series of functional proteins that support two types of infection, latent and lytic.