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Antiviral agents are used for the treatment of viral diseases. Antiviral drugs have been successfully developed and used clinically for a limited number of important human viral diseases notably caused by human immunodeficiency virus (HIV), hepatitis C virus (HCV), hepatitis B virus (HBV), herpes, and influenza viruses. Despite the successes of these antiviral drugs, issues with drug resistance and toxicity remain challenging. These challenges are driving research to identify new drug candidates and to investigate novel drug targets to develop new mechanistic drug classes. Antiviral agents are not available against many viruses that cause human disease and economic burdens; in particular, the development of antiviral agents against emerging, re-emerging, and neglected viruses is increasingly becoming a priority. This book includes six review articles that discuss new antiviral strategies. The reviews either discuss advances relating to a specific virus or new therapeutic targets and approaches. The book includes 15 original research articles reporting new antiviral agents against a variety of clinically and economically important viruses and studies into the prevalence or acquisition of drug resistance. Overall, this book is an exciting collection of new research and ideas relating to the development of antiviral agents.

Zika virus --- nucleoside analogues --- antiviral agents --- NS5 --- prodrugs --- ProTides --- neural stem cells --- RNA-dependent RNA polymerase --- cytomegalovirus --- latent infection --- TALEN --- Surveyor nuclease mutation detection assay --- ie-1 gene --- quantitative real-time PCR --- Epstein–Barr virus --- herpes viruses --- lytic gene expression --- Burkitt lymphoma cells --- clozapine --- antipsychotic drug --- antiviral drug --- enteroviruses --- coxsackievirus B4 --- persistent infection --- fluoxetine --- resistance --- mutations --- herpes B virus --- macacine herpesvirus-1 --- genistein --- flavonoids --- acyclovir --- ganciclovir --- Plantago asiatica --- Clerodendrum trichotomum --- RSV --- therapeutic effects --- acteoside --- human antimicrobial peptides --- antiviral strategies --- defensins --- cathelicidins --- hepcidins --- transferrins --- influenza A virus --- brevilin A --- antiviral --- sesquiterpene lactone --- replication --- PRRSV --- polyethylenimine --- PEI --- virion internalization --- endocytosis --- HIV --- pediatrics --- Ethiopia --- pre-treatment drug resistance --- combination antiretroviral therapy (cART) --- dried plasma spots --- dried blood spots --- sphingolipids --- glycosphingolipids --- viruses --- lipid biosynthesis --- flavivirus --- Japanese encephalitis virus --- furin inhibitor --- precursor membrane protein --- measles virus --- central nervous system --- tropism --- treatments --- porcine reproductive and respiratory syndrome virus --- ginsenoside Rg1 --- antiviral activity --- pro-inflammatory factor --- NF-κB signaling pathway --- acute/latent infection --- congenital infection --- antiviral agent --- therapeutic strategies --- nucleic acid-based therapeutic approach --- HCMV vaccine --- adoptive cell therapy --- Rev response element --- chemical footprinting --- SHAPE --- drug discovery --- branched peptides --- herpesvirus --- immediate-early --- IE1 --- IE2 --- ribozyme --- RNA interference --- CRISPR/Cas --- small molecule --- orthohantavirus --- phenyl-benzotriazoles --- C-FRA --- Porcine circovirus type 2 --- epigallocatechin gallate --- heparan sulfate --- antiviral effect --- virus attachment --- microvirin --- lectin --- human immunodeficiency virus --- hepatitis C virus --- antiviral inhibitor --- non-immunogenic --- viral entry --- protein drugs --- LUMS1 --- oleanane-type derivatives --- influenza A virus (IAV) --- virus entry inhibitors --- hemagglutinin (HA) --- n/a --- Epstein-Barr virus

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Every minute, 34 new patients are diagnosed with cancer globally. Although over the past 50 years treatments have improved and survival rates have increased dramatically for several types of cancers, many remain incurable. Several aggressive types of blood and solid cancers form when mutations occur in a critical cellular signaling pathway, the JAK-STAT pathway; (Janus Kinase-Signal Transducer and Activator of Transcription). Currently, there are no clinically available drugs that target the oncogenic STAT3/5 proteins in particular or their Gain of Function hyperactive mutant products. Here, we summarize targeting approaches on STAT3/5, as the field moves towards clinical applications as well as we illuminate on upstream or downstream JAK-STAT pathway interference with kinase inhibitors, heat shock protein blockers or changing nuclear import/export processes. We cover the design paradigms and medicinal chemistry approaches to illuminate progress and challenges in understanding the pleiotropic role of STAT3 and STAT5 in oncogenesis, the microenvironment, the immune system in particular, all culminating in a complex interplay towards cancer progression.

multiple myeloma --- STAT3 --- S3I-1757 --- nanoparticle --- CD38 --- siRNA/RNAi --- polyethylenimine --- PEI --- lipopolyplex --- siRNA delivery --- glioma --- glioblastoma --- STAT5 --- AKT --- ERK1/2 --- prolactin --- androgens --- prostate cancer --- knockout --- escape mechanisms --- stem/progenitor cells --- cell hierarchy --- cancer --- CD4+ T cells --- CD8+ T cells --- myeloid cells --- immune check point --- hepatitis C virus (HCV) --- cirrhosis --- hepatocellular carcinoma (HCC) --- endoplasmic reticulum (ER) stress --- oxidative stress (OS) --- unfolded protein response (UPR) --- microRNA-122 (miR-122) --- nuclear factor erythroid 2-related factor 2 (NRF2) --- signal transducer and activator of transcription 3 (STAT3) --- hepatocyte nuclear factor 4 alpha (HNF4A) --- solid cancers --- cell cycle --- apoptosis --- inflammation --- mitochondria --- stemness --- tumor suppression --- melanoma --- autoimmune disease --- immunotherapy --- tumor–immune cell interactions --- breast cancer --- PD-L1 --- M2 macrophages --- NK cells --- STAT3 inhibitor XIII --- hedging --- transaction costs --- dynamic programming --- risk management --- post-decision state variable --- cancer progression --- cancer-stem cell --- cytokine --- therapy resistance --- metastasis --- immunosuppression --- tumor microenvironment --- proliferation --- tyrosine kinase 2 --- JAK family of protein tyrosine kinases --- signal transducer and activator of transcription --- cytokine receptor signaling --- gain-of-function mutation --- tumorigenesis --- ADAM17 --- interleukin-6 --- trans-signaling --- epidermal growth factor receptor (EGF-R) --- shedding --- metalloprotease --- tumor necrosis factor alpha (TNFα) --- inflammation associated cancer --- colon cancer --- lung cancer --- SH2 domain --- mutations --- autosomal-dominant hyper IgE syndrome --- inflammatory hepatocellular adenomas --- T-cell large granular lymphocytic leukemia --- T-cell prolymphocytic leukemia --- growth hormone insensitivity syndrome --- nuclear pore complex --- nuclear transport receptors --- nucleocytoplasmic shuttling --- targeting --- tumor-associated macrophages --- adoptive T cell therapy --- immune suppression --- STAT transcription factors --- JAK --- STAT --- T-PLL --- T-cell leukemia --- meta-analysis --- STAT5B signaling --- small-molecule inhibitors --- cancer models --- companion animals --- comparative oncology --- pharmacological inhibitor --- STAT5 signaling --- chemotherapy resistance --- myeloid leukemia --- heat shock proteins --- chaperones --- stabilization --- targeted therapy --- ovarian cancer --- hematopoietic cancers --- therapeutic targeting --- pharmacological inhibitors --- mTOR --- Bone Marrow Failure Syndromes --- lymphocytes --- lymphoma --- T-cells --- RHOA --- NGS --- MPN --- JAK2 V617F --- neoplastic stem cells --- n/a --- tumor-immune cell interactions