The novel HLA-B*39:199 allele identified in a candidate bone marrow donor.

HLA-B*39:199 differs from HLA-B*39:10:01 by a G → A substitution in exon 5 in codon 282.

The IGSF1, Wnt5a, FGF14, and ITPR1 Gene Expression and Prognosis Hallmark of Prostate Cancer.

Background: Prostate cancer is considered as the second leading cause of cancer related death in men worldwide and the third frequent cancer among Iranian men. Despite the use of PSA as the only biomarker for early diagnosis of prostate cancer, its application in clinical settings is under debate. Therefore, the introduction of new molecular markers for early detection of prostate cancer is needed. Methods: In the present study we intended to evaluate the expression of IGSF1, Wnt5a, FGF14, and ITPR1 in prostate cancer specimens by real time PCR. Biopsy samples of 40 prostate cancer cases and 41 healthy Iranian men were compared to determine the relative gene expression of IGSF1, Wnt5a, FGF14, and ITPR1 by real time PCR. Results: Our results showed that Wnt5a, FGF14, and IGSF1 were significantly overexpressed in the prostate cancer patients while the mean relative expression of ITPR1 showed a significant decrease in PCa samples compared to healthy controls. Conclusion: According to results of the present study, the combination panel of IGSF1, Wnt5a, FGF14, and ITPR1 genes could be considered as potential genetic markers for prostate cancer diagnosis. However further studies on larger populations and investigating the clinicopathological relevance of these genes is needed.

SARS-CoV-2 and Guillain-Barré Syndrome: Lessons from Viral Infections.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the COVID-19 pandemic. COVID-19 has a broad clinical spectrum from asymptomatic patients to multiorgan dysfunction and septic shock. Most of the common symptoms of COVID-19 are classified as respiratory disorders, but some reports show neurological involvements. During the COVID-19 pandemic, a case series of neurological complications, such as Guillain-Barré syndrome (GBS), were reported. GBS is a neuroimmune disorder with acute inflammatory radicular polyneuropathy in different parts of the peripheral nerve. Some studies have reported GBS as an inflammatory neuropathy related to various viral infections, such as cytomegalovirus (CMV), Epstein-Barr Virus (EBV), herpes simplex virus (HSV), human immunodeficiency virus (HIV), influenza, and Zika virus. There are some immunomodulation approaches for the management of GBS. Studies have evaluated the effects of the various therapeutic approaches, including intravenous immunoglobulin (IVIG), plasma exchange (PE), complement inhibitors, and corticosteroids to regulate overactivation of immune responses during GBS in experimental and clinical studies. In this regard, the possible association between GBS and SARS-CoV-2 infection during the outbreak of the current pandemic and also the mentioned therapeutic approaches were reviewed.

Potential Antiviral Immune Response Against COVID-19: Lessons Learned from SARS-CoV.

Virus and host innate immune system interaction plays a significant role in forming the outcome of viral diseases. Host innate immunity initially recognizes the viral invasion and induces a rapid inflammatory response, and this recognition activates signaling cascades that trigger the release of antiviral mediators. This chapter aims to explore the mechanisms by which newly emerged coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) activates the host immune system. Since SARS-CoV-2 shares similarities with SARS-CoV that caused the epidemic of SARS in 2003, the pathogenesis of both viruses could be at least very similar. For this, this chapter provides a synthesis of literature concerning antiviral immunity in SARS-CoV and SARS-CoV-2. It includes the presentation of epitopes linked to SARS-CoV-2 as well as the ability of SARS-CoV-2 to cause proteolytic activation and interact with angiotensin-converting enzyme 2 (ACE2) via molecular mimicry. This chapter characterizes various mechanisms that this virus may engage in escaping the host immunity, ended by a discussion of humoral immune responses against SARS-CoV-2.