Japanese encephalitis (JE) disease, a viral brain fever is caused by Japanese encephalitis virus (JEV). Despite the availability of effective vaccines against this deadly infection, JE is the leading cause of epidemic viral encephalitis in children in South-east Asia. There is no treatment available for the JE disease which might be due to incomplete understanding of the pathogenesis of JE virus. The JEV infections lead to permanent neurological deficits even in those who survive from the infection. Activated microglia may play a potentially detrimental role by eliciting the expression of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) influencing the surrounding brain tissue. Microglial activation, proinflammatory cytokine release and leukocytes trafficking are associated following JEV infection in central nervous system (CNS). How the pattern recognition receptors sense the viral nucleic acid and how the microglial and neuronal cells behaves following JEV infection is still unelucidated. There is scarcity of data on the expression levels of toll like receptors (TLRs), cytokines and chemokines in JEV infection in invitro model. To explore the molecular mechanisms of JEV infection of microglial cells and neuronal cells, we studied the expression profile of TLRs, cytokines and chemokines in JEV infected microglial cell line BV2 and Neuronal cell line Neuro 2A. For the present study, we developed the mouse model of encephalitis by intracerebral (IC) injection of JE virus for virus propagation, disease progression and damage study. Our results demonstrate the exaggerated release of some specific TLRs, cytokines and chemokines in invitro cell culture of microglial and Neuro 2A cell line, which are associated with bad outcome in invivo study.

Acinetobacter spp., is an opportunistic, gram negative and non-fermenter organism, has occurred as one of the maximum bothersome pathogens for health care organisations worldwide. This organism generally targets the most susceptible hospitalized patients causing pneumonia mainly in patients on mechanical ventilation in ICU, having urinary tract infection, bloodstream infections, skin infections etc. It accounts for about 10% of all nosocomial infections. Its clinical significance over last 15 years has been forced by its amazing capacity to get resistant elements, making it one of the antagonistic organisms in the current antibiotic era. Most of Acinetobacter strains are resistant to all known antibiotics have been reported and they are acting in interaction with this emerging resistance profile, with this ability. Acinetobacter isolatesare able to survive for long periods throughout the hospital environment. Itrecurrently causes infections associated with medical devices, e.g. vascular catheters, cerebrospinal fluid shunts, urinary catheter or an endotracheal tube. Microbial biofilms are considered as virulence factors and is a well-known pathogenic mechanism in such infections. The ability to form biofilms on biotic or abiotic surfaces is a common trait among Acinetobacter strains. Therefore, the present study was undertaken to study antibiotic resistance patterns and association the resistance profile with bio-film production in various clinical isolates of Acinetobacter spp. A total of 35 isolates of Acinetobacter species were obtained for study from various clinical specimens like pus, urine, sputum, blood culture specimens from the patients admitted in hospital. Isolates obtained from different medical specimens were managed and confirmed by conservative microbiological procedures. The isolates of Acinetobacter are identified on the basis of certain biochemical test like catalase positive, oxidase negative, urease negative, nitrate negative, indole negative and non-motility test. A total of 35 isolates were subjected to susceptibility testing by disc diffusion method according to CLSI guidelines for 14 clinically relevant antibiotics. Screening for biofilm production was done quantitatively by micro titre plate assay method. In the present study, 75% isolates were showing antibiotic resistance and 22.8% isolates produced bio film along with antibiotic resistance. Biofilm formers isolates showed high resistance to imipenem, cephotaxime, ceftazidime, tobramycin, ciprofloxacin as compared to nonbiofilm formers. We selected to study the biofilm formation and antibiotic resistance of clinical isolates of Acinetobacter species to understand its ability to persist in the hospital environment to cause outbreaks.

Acute kidney infection (AKI) occurred by tubular necrosis and glomerular dysfunction caused by many factors. SARS CoV-2 infection identified to cause fatal AKI. This paper aims to review the effect of covid-19 infection on the failure of the kidney and its mechanism. It identified that the SARS-CoV-2 received by the targeted cell by Angiotensin-converting enzyme 2 (ACE2). After the virus received by the target cells, it induces the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-1, and interferons (IFN) by immune cells and causes cytokine storm. The pro-inflammatory cytokines are again responsible to induce the secretion of cyclooxygenase‑2 (COX‑2), which causes inflammation and pain as well it stimulates the iNOS enzyme to produce NO which allows the vasodilation of renal arteries. The increased production of NO by iNO enhanced the vasodilation of arteries, and allows the adhesion of neutrophils to the artery, and causes damage to glomerulus and tubules. Hence, the most likely sustainable intervention could be the application of angiotensin-converting enzyme 2 (ACE2) inhibition by the receptors of the target cells in these vital organs to reduce sever destruction during treatment at the early stage of infection.