CRISPR/Cas9 engineered viral immunity in plants

Author(s):  
Dharmendra Pratap ◽  
Ankit Kumar
Keyword(s):  
Author(s):  
Kristen Orumaa ◽  
Margaret R. Dunne

AbstractCOVID-19 is a respiratory disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was first documented in late 2019, but within months, a worldwide pandemic was declared due to the easily transmissible nature of the virus. Research to date on the immune response to SARS-CoV-2 has focused largely on conventional B and T lymphocytes. This review examines the emerging role of unconventional T cell subsets, including γδ T cells, invariant natural killer T (iNKT) cells and mucosal associated invariant T (MAIT) cells in human SARS-CoV-2 infection.Some of these T cell subsets have been shown to play protective roles in anti-viral immunity by suppressing viral replication and opsonising virions of SARS-CoV. Here, we explore whether unconventional T cells play a protective role in SARS-CoV-2 infection as well. Unconventional T cells are already under investigation as cell-based immunotherapies for cancer. We discuss the potential use of these cells as therapeutic agents in the COVID-19 setting. Due to the rapidly evolving situation presented by COVID-19, there is an urgent need to understand the pathogenesis of this disease and the mechanisms underlying its immune response. Through this, we may be able to better help those with severe cases and lower the mortality rate by devising more effective vaccines and novel treatment strategies.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Weinan Qiu ◽  
Qingyang Zhang ◽  
Rui Zhang ◽  
Yangxu Lu ◽  
Xin Wang ◽  
...  

AbstractDouble-stranded RNA (dsRNA) is a virus-encoded signature capable of triggering intracellular Rig-like receptors (RLR) to activate antiviral signaling, but whether intercellular dsRNA structural reshaping mediated by the N6-methyladenosine (m6A) modification modulates this process remains largely unknown. Here, we show that, in response to infection by the RNA virus Vesicular Stomatitis Virus (VSV), the m6A methyltransferase METTL3 translocates into the cytoplasm to increase m6A modification on virus-derived transcripts and decrease viral dsRNA formation, thereby reducing virus-sensing efficacy by RLRs such as RIG-I and MDA5 and dampening antiviral immune signaling. Meanwhile, the genetic ablation of METTL3 in monocyte or hepatocyte causes enhanced type I IFN expression and accelerates VSV clearance. Our findings thus implicate METTL3-mediated m6A RNA modification on viral RNAs as a negative regulator for innate sensing pathways of dsRNA, and also hint METTL3 as a potential therapeutic target for the modulation of anti-viral immunity.


1977 ◽  
Vol 32 (2) ◽  
pp. 153-167 ◽  
Author(s):  
G.J Stewart ◽  
A Basten ◽  
J Guinan ◽  
H.V Bashir ◽  
J Cameron ◽  
...  

2013 ◽  
Vol 15 (6) ◽  
Author(s):  
John M Davis ◽  
Keith L Knutson ◽  
Michael A Strausbauch ◽  
Abigail B Green ◽  
Cynthia S Crowson ◽  
...  

1998 ◽  
Vol 8 (14) ◽  
pp. R498-R501 ◽  
Author(s):  
David F. Tough ◽  
Jonathan Sprent
Keyword(s):  
T Cells ◽  

2004 ◽  
Vol 82 (3) ◽  
pp. 332-341 ◽  
Author(s):  
Serani LH Dommelen ◽  
Mariapia A Degli‐Esposti
Keyword(s):  

2021 ◽  
Author(s):  
Maya M.L. Poon ◽  
Eve Byington ◽  
Wenzhao Meng ◽  
Masaru Kubota ◽  
Rei Matsumoto ◽  
...  
Keyword(s):  

2021 ◽  
Vol 17 (3) ◽  
pp. e1009324
Author(s):  
Lucas dos Santos Dias ◽  
Hannah E. Dobson ◽  
Brock Kingstad Bakke ◽  
Gregory C. Kujoth ◽  
Junfeng Huang ◽  
...  

The development of safe subunit vaccines requires adjuvants that augment immunogenicity of non-replicating protein-based antigens. Current vaccines against infectious diseases preferentially induce protective antibodies driven by adjuvants such as alum. However, the contribution of antibody to host defense is limited for certain classes of infectious diseases such as fungi, whereas animal studies and clinical observations implicate cellular immunity as an essential component of the resolution of fungal pathogens. Here, we decipher the structural bases of a newly identified glycoprotein ligand of Dectin-2 with potent adjuvancy, Blastomyces endoglucanase-2 (Bl-Eng2). We also pinpoint the developmental steps of antigen-specific CD4+ and CD8+ T responses augmented by Bl-Eng2 including expansion, differentiation and tissue residency. Dectin-2 ligation led to successful systemic and mucosal vaccination against invasive fungal infection and Influenza A infection, respectively. O-linked glycans on Bl-Eng2 applied at the skin and respiratory mucosa greatly augment vaccine subunit- induced protective immunity against lethal influenza and fungal pulmonary challenge.


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