Insights into Acute Pancreatitis Associated COVID-19: Literature Review.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) primarily affects the lungs, causing respiratory symptoms. However, the infection clearly affects all organ systems including the gastrointestinal system. Acute pancreatitis associated with coronavirus disease 2019 (COVID-19) has been widely reported Recent studies have discussed pancreatic compromise incidentally in asymptomatic patients, or in a form of clinical symptoms such as abdominal pain, nausea, or vomiting, which is further reflected in some cases with abnormal serum lipase and amylase levels It was suggested that upregulation of angiotensin-converting enzyme II cell receptors or inflammatory cytokines play a major role in predisposing pancreatic injury in SARS-CoV-2 positive patients To date, there is insufficient data to establish the causality of acute pancreatitis in SARS-CoV-2 infected cases. In this paper, we organize recent studies conducted to observe the frequency of acute pancreatitis associated with COVID-19 cases while highlighting present hypotheses, predisposing factors, and their effect on the outcome, and point to gaps in our knowledge.

Response to Penicillin for Presumed Neurosyphilis in a Patient with Human Immunodeficiency Virus (HIV), a Normal CD4 Count, and an Undetectable Viral Load: A Case Report.

BACKGROUND Neurosyphilis is a bacterial infection of the brain and the spinal cord, caused by Treponema pallidum. Its nonspecific clinical presentation includes cognitive impairment and motor and/or sensory function compromise. Neurosyphilis infections in patients with HIV have increased over the past few years and many cases of neurosyphilis manifest in patients with HIV who have low CD4 T-cell counts and high viral loads (VL). However, there is extremely limited acknowledgement in the literature about neurosyphilis presentations in patients with HIV who have normal CD4 counts. CASE REPORT We present a neurosyphilis and HIV coinfection in a patient with a normal CD4 count and an undetectable VL. A 69-year-old woman with a medical history of HIV was on a prescribed antiretroviral treatment regimen. She presented in the Emergency Room in an unresponsive state, although this had been preceded by a period of rapidly progressive cognitive decline. Her brain computed tomography scan without contrast was unremarkable. Laboratory test results were within normal limits, except for a positive result for the microhemagglutination assay for Treponema pallidum antibodies and rapid plasma regain (RPR) test, which was highly suggestive of neurosyphilis as a presumed diagnosis. She showed remarkable clinical improvement after the initiation of conventional treatment for neurosyphilis, which is a 14-day regimen of intravenous penicillin G. CONCLUSIONS Given the broad neurological manifestations of neurosyphilis and its increasing incidence in patients with HIV, it is important to consider neurosyphilis in the differential diagnosis after ruling out other causes of encephalopathy, especially in patients with an undetectable VL and a normal CD4 count.

Crystal structure of adenovirus E3-19K bound to HLA-A2 reveals mechanism for immunomodulation.

E3-19K binds to and retains MHC class I molecules in the endoplasmic reticulum, suppressing anti-adenovirus activities of T cells. We determined the structure of the adenovirus serotype 2 (Ad2, species C) E3-19K-HLA-A2 complex to 1.95-Å resolution. Ad2 E3-19K binds to the N terminus of the HLA-A2 groove, contacting the α1, α2 and α3 domains and ß(2)m. Ad2 E3-19K has a unique structure comprising a large N-terminal domain, formed by two partially overlapping ß-sheets arranged in a V shape, and a C-terminal α-helix and tail. The structure reveals determinants in E3-19K and HLA-A2 that are important for complex formation; conservation of some of these determinants in E3-19K proteins of different species and MHC I molecules of different loci suggests a universal binding mode for all E3-19K proteins. Our structure is important for understanding the immunomodulatory function of E3-19K.