Acquired Angioedema Post COVID-19 Infection: Can SARS-Cov-2 Induce Angioedema?

Ongoing research continues to uncover the long-term effects of post-COVID-19 illnesses. Patients with hereditary angioedema (HAE) are believed to have an elevated risk of contracting COVID-19 caused by SARS-CoV-2, potentially leading to increased frequency or more severe symptoms. This speculation is based on the understanding that COVID-19 enters cells through the angiotensin-converting enzyme 2 (ACE2) receptor.

Hemophagocytic Lymphohistiocytosis in Visceral Leishmaniasis: A Rare yet Treatable Complication.

Hemophagocytic lymphohistiocytosis (HLH) is a rare debilitating condition that can be triggered by an infectious cause, often linked to the Epstein-Barr virus (EBV). In this case, we evaluated a patient with pancytopenia. The bone marrow aspiration revealed the presence of amastigotes and active hemophagocytosis, indicating that the HLH was induced by a infection.

Prevalence of pelvic examinations on anesthetized patients without informed consent.

Context: The pelvic examination is a fundamental tool for the evaluation and diagnosis of women's health conditions and an important skill for all medical students to learn as future physicians for the early detection of treatable conditions such as infection or cancer. Although the American College of Obstetricians and Gynecologists (ACOG) asserts that performing pelvic examinations under anesthesia for educational purposes should only occur if the patient provides explicit and informed consent, there still have been reports of medical students performing pelvic examinations on anesthetized patients across the country, and many states are now starting to pass bills requiring informed patient consents to conduct pelvic examinations under anesthesia.

Objectives: The objectives of this study are to evaluate the prevalence of pelvic examinations performed by osteopathic medical students on anesthetized patients without consent while fulfilling their third-year OB-GYN clerkship requirements.

HIV-1-induced nuclear invaginations mediated by VAP-A, ORP3, and Rab7 complex explain infection of activated T cells.

The mechanism of human immunodeficiency virus 1 (HIV-1) nuclear entry, required for productive infection, is not fully understood. Here, we report that in HeLa cells and activated CD4 T cells infected with HIV-1 pseudotyped with VSV-G and native Env protein, respectively, Rab7 late endosomes containing endocytosed HIV-1 promote the formation of nuclear envelope invaginations (NEIs) by a molecular mechanism involving the VOR complex, composed of the outer nuclear membrane protein VAP-A, hyperphosphorylated ORP3 and Rab7. Silencing VAP-A or ORP3 and drug-mediated impairment of Rab7 binding to ORP3-VAP-A inhibited the nuclear transfer of the HIV-1 components and productive infection.

Barriers to research opportunities among osteopathic medical students.

Context: Despite the increase of importance placed on research, both by residency program directors and the medical field at large, osteopathic medical students (OMS) have significantly fewer research experiences than United States (U.S.) allopathic medical students and non-U.

Modulation of hepatitis C virus genome encapsidation by nonstructural protein 4B.

Hepatitis C Virus (HCV) NS4B protein has many roles in HCV genome replication. Recently, our laboratory (Q. Han, J.

Conserved GXXXG- and S/T-like motifs in the transmembrane domains of NS4B protein are required for hepatitis C virus replication.

Hepatitis C virus (HCV) nonstructural protein 4B (NS4B) is an integral membrane protein, which plays an important role in the organization and function of the HCV replication complex (RC). Although much is understood about its amphipathic N-terminal and C-terminal domains, we know very little about the role of the transmembrane domains (TMDs) in NS4B function. We hypothesized that in addition to anchoring NS4B into host membranes, the TMDs are engaged in intra- and intermolecular interactions required for NS4B structure/function.

Autophagy protein ATG5 interacts transiently with the hepatitis C virus RNA polymerase (NS5B) early during infection.

Autophagy is an important cellular process by which ATG5 initiates the formation of double membrane vesicles (DMVs). Upon infection, DMVs have been shown to harbor the replicase complex of positive-strand RNA viruses such as MHV, poliovirus, and equine arteritis virus. Recently, it has been shown that autophagy proteins are proviral factors that favor initiation of hepatitis C virus (HCV) infection.

Endocytic Rab proteins are required for hepatitis C virus replication complex formation.

During infection, hepatitis C virus (HCV) NS4B protein remodels host membranes to form HCV replication complexes (RC) which appear as foci under fluorescence microscopy (FM). To understand the role of Rab proteins in forming NS4B foci, cells expressing the HCV replicon were examined biochemically and via FM. First, we show that an isolated NS4B-bound subcellular fraction is competent for HCV RNA synthesis.

Formation and function of hepatitis C virus replication complexes require residues in the carboxy-terminal domain of NS4B protein.

During replication, hepatitis C virus (HCV) NS4B protein rearranges intracellular membranes to form foci, or the web, the putative site for HCV replication. To understand the role of the C-terminal domain (CTD) in NS4B function, mutations were introduced into NS4B alone or in the context of HCV polyprotein. First, we show that the CTD is required for NS4B-induced web structure, but it is not sufficient to form the web nor is it required for NS4B membrane association.

Role of the hydrophilic channels of simian virus 40 T-antigen helicase in DNA replication.

The simian virus 40 (SV40) hexameric helicase consists of a central channel and six hydrophilic channels located between adjacent large tier domains within each hexamer. To study the function of the hydrophilic channels in SV40 DNA replication, a series of single-point substitutions were introduced at sites not directly involved in protein-protein contacts. The mutants were characterized biochemically in various ways.