scholarly journals Lymphopenia Caused by Virus Infections and the Mechanisms Beyond

Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1876
Author(s):  
Zijing Guo ◽  
Zhidong Zhang ◽  
Meera Prajapati ◽  
Yanmin Li
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Clinical Course ◽  
Detailed Knowledge ◽  
Virus Infections ◽  
Adaptive Immune Responses ◽  
Therapeutic Targeting ◽  
Adaptive Immune

Viral infections can give rise to a systemic decrease in the total number of lymphocytes in the blood, referred to as lymphopenia. Lymphopenia may affect the host adaptive immune responses and impact the clinical course of acute viral infections. Detailed knowledge on how viruses induce lymphopenia would provide valuable information into the pathogenesis of viral infections and potential therapeutic targeting. In this review, the current progress of viruses-induced lymphopenia is summarized and the potential mechanisms and factors involved are discussed.

scholarly journals Interferon-Mediated Immunopathological Events Are Associated with Atypical Innate and Adaptive Immune Responses in Patients with Severe Acute Respiratory Syndrome

2007 ◽  
Vol 81 (16) ◽  
pp. 8692-8706 ◽  
Author(s):  
Mark J. Cameron ◽  
Longsi Ran ◽  
Luoling Xu ◽  
Ali Danesh ◽  
Jesus F. Bermejo-Martin ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Immune Responses ◽  
Viral Infections ◽  
Fatal Outcome ◽  
Careful Examination ◽  
Type I ◽  
Immunoglobulin Gene ◽  
Adaptive Immune Responses ◽  
Immune Genes ◽  
Adaptive Immune

ABSTRACT It is not understood how immune inflammation influences the pathogenesis of severe acute respiratory syndrome (SARS). One area of strong controversy is the role of interferon (IFN) responses in the natural history of SARS. The fact that the majority of SARS patients recover after relatively moderate illness suggests that the prevailing notion of deficient type I IFN-mediated immunity, with hypercytokinemia driving a poor clinical course, is oversimplified. We used proteomic and genomic technology to systematically analyze host innate and adaptive immune responses of 40 clinically well-described patients with SARS during discrete phases of illness from the onset of symptoms to discharge or a fatal outcome. A novel signature of high IFN-α, IFN-γ, and IFN-stimulated chemokine levels, plus robust antiviral IFN-stimulated gene (ISG) expression, accompanied early SARS sequelae. As acute illness progressed, SARS patients entered a crisis phase linked to oxygen saturation profiles. The majority of SARS patients resolved IFN responses at crisis and expressed adaptive immune genes. In contrast, patients with poor outcomes showed deviated ISG and immunoglobulin gene expression levels, persistent chemokine levels, and deficient anti-SARS spike antibody production. We contend that unregulated IFN responses during acute-phase SARS may culminate in a malfunction of the switch from innate immunity to adaptive immunity. The potential for the use of the gene signatures we describe in this study to better assess the immunopathology and clinical management of severe viral infections, such as SARS and avian influenza (H5N1), is therefore worth careful examination.

scholarly journals MiR-146a in Immunity and Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Nicole Rusca ◽  
Silvia Monticelli
Keyword(s):  
Immune Responses ◽  
Recent Progress ◽  
Viral Infections ◽  
Cellular Functions ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Different Types ◽  
A Cell ◽  
And Function

MicroRNAs (miRNAs) are regulatory molecules able to influence all aspects of the biology of a cell. They have been associated with diseases such as cancer, viral infections, and autoimmune diseases, and in recent years, they also emerged as important regulators of immune responses. MiR-146a in particular is rapidly gaining importance as a modulator of differentiation and function of cells of the innate as well as adaptive immunity. Given its importance in regulating key cellular functions, it is not surprising that miR-146a expression was also found dysregulated in different types of tumors. In this paper, we summarize recent progress in understanding the role of miR-146a in innate and adaptive immune responses, as well as in disease.

scholarly journals Toll-Like Receptors: Are They Taking a Toll on the Heart in Viral Myocarditis?

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1003
Author(s):  
Kasper Favere ◽  
Matthias Bosman ◽  
Karin Klingel ◽  
Stephane Heymans ◽  
Sophie Van Linthout ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Viral Myocarditis ◽  
Disease Process ◽  
Future Research ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Evolutionarily Conserved

Myocarditis is an inflammatory disease of the heart with viral infections being the most common aetiology. Its complex biology remains poorly understood and its clinical management is one of the most challenging in the field of cardiology. Toll-like receptors (TLRs), a family of evolutionarily conserved pattern recognition receptors, are increasingly known to be implicated in the pathophysiology of viral myocarditis. Their central role in innate and adaptive immune responses, and in the inflammatory reaction that ensues, indeed makes them prime candidates to profoundly affect every stage of the disease process. This review describes the pathogenesis and pathophysiology of viral myocarditis and scrutinises the role of TLRs in every phase. We conclude with directions for future research in this field.

scholarly journals Regulation of Antiviral Immune Response by N6-Methyladenosine of mRNA

2021 ◽  
Vol 12 ◽  
Author(s):  
Baoxin Zhao ◽  
Weijie Wang ◽  
Yan Zhao ◽  
Hongxiu Qiao ◽  
Zhiyun Gao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infection ◽  
Viral Infections ◽  
Immune Cell ◽  
Vital Role ◽  
Immune Defense ◽  
Interferon Response ◽  
Adaptive Immune Responses ◽  
Antiviral Immune Response ◽  
Adaptive Immune

Host innate and adaptive immune responses play a vital role in clearing infected viruses. Meanwhile, viruses also evolve a series of mechanisms to weaken the host immune responses and evade immune defense. Recently, N6-methyladenosine (m6A), the most prevalent mRNA modification, has been revealed to regulate multiple steps of RNA metabolism, such as mRNA splicing, localization, stabilization, and translation, thus participating in many biological phenomena, including viral infection. In the process of virus–host interaction, the m6A modification that presents on the virus RNA impedes capture by the pattern recognition receptors, and the m6A modification appearing on the host immune-related molecules regulate interferon response, immune cell differentiation, inflammatory cytokine production, and other immune responses induced by viral infection. This review summarizes the research advances about the regulatory role of m6A modification in the innate and adaptive immune responses during viral infections.

scholarly journals The Inability of Wild-Type Rabies Virus To Activate Dendritic Cells Is Dependent on the Glycoprotein and Correlates with Its Low Level of theDe Novo-Synthesized Leader RNA

2014 ◽  
Vol 89 (4) ◽  
pp. 2157-2169 ◽  
Author(s):  
Yang Yang ◽  
Ying Huang ◽  
Clement W. Gnanadurai ◽  
Shengbo Cao ◽  
Xueqin Liu ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Rabies Virus ◽  
Adoptive Transfer ◽  
Viral Infections ◽  
De Novo ◽  
Wild Type ◽  
Adaptive Immune Responses ◽  
Low Level ◽  
Adaptive Immune

ABSTRACTDendritic cells (DCs) are the most efficient antigen-presenting cells, playing a key role in the adaptive immune responses to viral infections. Our studies demonstrate that wild-type (wt) rabies virus (RABV) does not activate DCs. Adoptive transfer of DCs primed with wt RABV did not activate DCs, stimulate virus neutralizing antibodies (VNA), or protect recipients against challenge. However, adoptive transfer of DCs primed with laboratory-attenuated RABV resulted in DC activation, production of VNA, and protection against challenge.In vitrostudies with recombinant RABV (laboratory-attenuated RABV expressing the glycoprotein or the phosphoprotein from wt RABV) demonstrate that DC activation is dependent on the glycoprotein and involves the IPS-1 pathway. Furthermore, binding to and entry into DCs by wt RABV is severely blocked, and the copy number ofde novo-synthesized leader RNA was two logs lower in DCs infected with the wt than in DCs treated with laboratory-attenuated RABV. However, transient transfection of DCs with synthesized leader RNA from either wt or attenuated RABV is capable of activating DCs in a dose-dependent manner. Thus, the inability of wt RABV to activate DCs correlates with its low level of thede novo-synthesized leader RNA.IMPORTANCERabies remains a public health threat, with more than 55,000 fatalities each year around the world. Since DCs play a key role in the adaptive immune responses to viral infections, we investigated the ability of rabies virus (RABV) to activate DCs. It was found that the adoptive transfer of DCs primed with wt RABV did not activate DCs, stimulate VNA, or protect mice against lethal challenge. However, laboratory-attenuated RABV mediates the activation of DCs via the IPS-1 pathway and is glycoprotein dependent. We further show that wt RABV evades DC-mediated immune activation by inefficient binding/entry into DCs and as a result of a reduced level ofde novo-synthesized leader RNA. These findings may have important implications in the development of efficient rabies vaccines.

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