Nipah (Nee-pa) viral disease is a zoonotic infection caused by Nipah virus (NiV), a paramyxovirus belonging to the genus Henipavirus of the family Paramyxoviridae. It is a biosafety level-4 pathogen, which is transmitted by specific types of fruit bats, mainly Pteropus spp. which are natural reservoir host. The disease was reported for the first time from the Kampung Sungai Nipah village of Malaysia in 1998. Human-to-human transmission also occurs. Outbreaks have been reported also from other countries in South and Southeast Asia. Phylogenetic analysis affirmed the circulation of two major clades of NiV as based on currently available complete N and G gene sequences. NiV isolates from Malaysia and Cambodia clustered together in NiV-MY clade, whereas isolates from Bangladesh and India clusterered within NiV-BD clade. NiV isolates from Thailand harboured mixed population of sequences. In humans, the virus is responsible for causing rapidly progressing severe illness which might be characterized by severe respiratory illness and/or deadly encephalitis. In pigs below six months of age, respiratory illness along with nervous symptoms may develop. Different types of enzyme-linked immunosorbent assays along with molecular methods based on polymerase chain reaction have been developed for diagnostic purposes. Due to the expensive nature of the antibody drugs, identification of broad-spectrum antivirals is essential along with focusing on small interfering RNAs (siRNAs). High pathogenicity of NiV in humans, and lack of vaccines or therapeutics to counter this disease have attracted attention of researchers worldwide for developing effective NiV vaccine and treatment regimens.

Various internal and external factors negatively affect the homeostatic equilibrium of organisms at the molecular to the whole-body level, inducing the so-called state of stress. Stress affects an organism's welfare status and induces energy-consuming mechanisms to combat the subsequent ill effects; thus, the individual may be immunocompromised, making them vulnerable to pathogens. The information presented here has been extensively reviewed, compiled, and analyzed from authenticated published resources available on Medline, PubMed, PubMed Central, Science Direct, and other scientific databases. Stress levels can be monitored by the quantitative and qualitative measurement of biomarkers. Potential markers of stress include thermal stress markers, such as heat shock proteins (HSPs), innate immune markers, such as Acute Phase Proteins (APPs), oxidative stress markers, and chemical secretions in the saliva and urine. In addition, stress biomarkers also play critical roles in the prognosis of stress-related diseases and disorders, and therapy guidance. Moreover, different components have been identified as potent mediators of cardiovascular, central nervous system, hepatic, and nephrological disorders, which can also be employed to evaluate these conditions precisely, but with stringent validation and specificity. Considerable scientific advances have been made in the detection, quantitation, and application of these biomarkers. The present review describes the current progress of identifying biomarkers, their prognostic, and therapeutic values.

Autophagy (self-eating) is a conserved cellular degradation process that plays important roles in maintaining homeostasis and preventing nutritional, metabolic, and infection-mediated stresses. Autophagy dysfunction can have various pathological consequences, including tumor progression, pathogen hyper-virulence, and neurodegeneration. This review describes the mechanisms of autophagy and its associations with other cell death mechanisms, including apoptosis, necrosis, necroptosis, and autosis. Autophagy has both positive and negative roles in infection, cancer, neural development, metabolism, cardiovascular health, immunity, and iron homeostasis. Genetic defects in autophagy can have pathological consequences, such as static childhood encephalopathy with neurodegeneration in adulthood, Crohn’s disease, hereditary spastic paraparesis, Danon disease, X-linked myopathy with excessive autophagy, and sporadic inclusion body myositis. Further studies on the process of autophagy in different microbial infections could help to design and develop novel therapeutic strategies against important pathogenic microbes. This review on the progress and prospects of autophagy research describes various activators and suppressors, which could be used to design novel intervention strategies against numerous diseases and develop therapeutic drugs to protect human and animal health.

In recent years, aquaculture has attained a major economic revolution, however, infectious diseases of bacterial, viral, mycotic and parasitic origin are the most significant restrictive agents in the improvement of intensified aquaculture, which has become a fast blooming seafood industry. For environment-friendly aquaculture and human health concerns owing to the rise in incidences of antimicrobial resistant microbes and food safety hazards, the immunoprophylaxis or vaccination strategies are highly effective and economical in protecting the health of fish and aquaculture animals from various infectious agents. Advancements in science have paved newer avenues in both basic and applied research areas for developing and designing novel and effective vaccines, as well as improving existing vaccines for rendering protection from various types of infectious diseases. Current advances in vaccines and vaccinology offer valuable opportunities to discover new vaccine candidates to combat fish pathogens, including mycotic and parasitic agents, for which vaccines are still lacking. This review focuses on the current knowledge, recent advances and future perspectives of vaccines and vaccination in the aquaculture industry, from traditional inactivated and attenuated vaccines to new generation vaccines comprising of recombinant, subunit, vectored, genetically engineered, DNA and peptide vaccines, reverse vaccinology and plant-based edible vaccines, and nanovaccines.

A recent outbreak of Nipah virus (NiV) in India has caused 17 deaths in people living in districts of Kerala state. Its zoonotic nature, as well as high rate of human-to-human transmission, has led researchers worldwide to work toward understanding the different aspects of the NiV. We performed a codon usage analysis, based on publicly available nucleotide sequences of NiV and its host adaptation, along with other members of the Henipavirus genus in ten hosts. NiV genome encodes nine open reading frames; and overall, no significant bias in codon usage was observed. Aromaticity of proteins had no impact on codon usage. An analysis of preferred codons used by NiV and the tRNA pool in human cells indicated that NiV prefers codons from a suboptimal anticodon tRNA pool. We observed that codon usage by NiV is mainly constrained by compositional and selection pressures, not by mutational forces. Parameters that define NiV and host relatedness in terms of codon usage were analyzed, with a codon adaptation index (CAI), relative codon deoptimization index (RCDI), and similarity index calculations; which indicated that, of all hosts analyzed, NiV was best adapted to African green monkeys. A comparative analysis based on the relative codon deoptimization index (RCDI) for host adaptation of NiV, Hendra virus (HeV), Cedar virus (CedV), and Hendra like Mojiang virus (MojV) revealed that except for dogs and ferrets, all evaluated hosts were more susceptible to HeV than NiV.

Antibody-dependent enhancement (ADE) is a phenomenon in which preexisting poorly neutralizing antibodies leads to enhanced infection. It is a serious concern with mosquito-borne flaviviruses such as Dengue virus (DENV) and Zika virus (ZIKV). In vitro experimental evidences have indicated the preventive, as well as a pathogenicity-enhancing role, of preexisting DENV antibodies in ZIKV infections. ADE has been confirmed in DENV but not ZIKV infections. Principally, the Fc region of the anti-DENV antibody binds with the fragment crystallizable gamma receptor (FcγR), and subsequent C1q interactions and immune effector functions are responsible for the ADE. In contrast to normal DENV infections, with ADE in DENV infections, inhibition of STAT1 phosphorylation and a reduction in IRF-1 gene expression, NOS2 levels, and RIG-1 and MDA-5 expression levels occurs. FcγRIIA is the most permissive FcγR for DENV-ADE, and under hypoxic conditions, hypoxia-inducible factor-1 alpha transcriptionally enhances expression levels of FcγRIIA, which further enhances ADE. To produce therapeutic antibodies with broad reactivity to different DENV serotypes, as well as to ZIKV, bispecific antibodies, Fc region mutants, modified Fc regions, and anti-idiotypic antibodies may be engineered. An in-depth understanding of the immunological and molecular mechanisms of DENV-ADE of ZIKV pathogenicity will be useful for the design of common and safe therapeutics and prophylactics against both viral pathogens. The present review discusses the role of DENV antibodies in modulating DENV/ZIKV pathogenicity/infection and strategies to counter ADE to protect against Zika infection.