viral infection
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2022 ◽  
Vol 3 (1) ◽  
pp. 101080
Zhenzhen Yan ◽  
Hansen Liu ◽  
Chengjiang Gao

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 143
Mithun Das ◽  
Monique L. Smith ◽  
Tomomi Furihata ◽  
Subir Sarker ◽  
Ross O’Shea ◽  

Zika virus (ZIKV) is a pathogenic neurotropic virus that infects the central nervous system (CNS) and results in various neurological complications. Astrocytes are the dominant CNS cell producer of the antiviral cytokine IFN-β, however little is known about the factors involved in their ability to mediate viral infection control. Recent studies have displayed differential responses in astrocytes to ZIKV infection, and this study sought to elucidate astrocyte cell-specific responses to ZIKV using a variety of cell models infected with either the African (MR766) or Asian (PRVABC59) ZIKV strains. Expression levels of pro-inflammatory (TNF-α and IL-1β) and inflammatory (IL-8) cytokines following viral infection were low and mostly comparable within the ZIKV-resistant and ZIKV-susceptible astrocyte models, with better control of proinflammatory cytokines displayed in resistant astrocyte cells, synchronising with the viral infection level at specific timepoints. Astrocyte cell lines displaying ZIKV-resistance also demonstrated early upregulation of multiple antiviral genes compared with susceptible astrocytes. Interestingly, pre-stimulation of ZIKV-susceptible astrocytes with either poly(I:C) or poly(dA:dT) showed efficient protection against ZIKV compared with pre-stimulation with either recombinant IFN-β or IFN-λ, perhaps indicating that a more diverse antiviral gene expression is necessary for astrocyte control of ZIKV, and this is driven in part through interferon-independent mechanisms.

ACS Omega ◽  
2022 ◽  
Barbara Vörös-Horváth ◽  
Pavo Živković ◽  
Krisztina Bánfai ◽  
Judit Bóvári-Biri ◽  
Judit Pongrácz ◽  

Mathematics ◽  
2022 ◽  
Vol 10 (2) ◽  
pp. 256
Latifa Ait Mahiout ◽  
Bogdan Kazmierczak ◽  
Vitaly Volpert

A new model of viral infection spreading in cell cultures is proposed taking into account virus mutation. This model represents a reaction-diffusion system of equations with time delay for the concentrations of uninfected cells, infected cells and viral load. Infection progression is characterized by the virus replication number Rv, which determines the total viral load. Analytical formulas for the speed of propagation and for the viral load are obtained and confirmed by numerical simulations. It is shown that virus mutation leads to the emergence of a new virus variant. Conditions of the coexistence of the two variants or competitive exclusion of one of them are found, and different stages of infection progression are identified.

2022 ◽  
Luisa Santus ◽  
Raquel García-Pérez ◽  
Maria Sopena-Rios ◽  
Aaron E Lin ◽  
Gordon C Adams ◽  

Long non-coding RNAs (lncRNAs) are pivotal mediators of systemic immune response to viral infection, yet most studies concerning their expression and functions upon immune stimulation are limited to in vitro bulk cell populations. This strongly constrains our understanding of how lncRNA expression varies at single-cell resolution, and how their cell-type specific immune regulatory roles may differ compared to protein-coding genes. Here, we perform the first in-depth characterization of lncRNA expression variation at single-cell resolution during Ebola virus (EBOV) infection in vivo. Using bulk RNA-sequencing from 119 samples and 12 tissue types, we significantly expand the current macaque lncRNA annotation. We then profile lncRNA expression variation in immune circulating single-cells during EBOV infection and find that lncRNAs' expression in fewer cells is a major differentiating factor from their protein-coding gene counterparts. Upon EBOV infection, lncRNAs present dynamic and mostly cell-type specific changes in their expression profiles especially in monocytes, the main cell type targeted by EBOV. Such changes are associated with gene regulatory modules related to important innate immune responses such as interferon response and purine metabolism. Within infected cells, several lncRNAs have positively and negatively correlated expression with viral load, suggesting that expression of some of these lncRNAs might be directly hijacked by EBOV to attack host cells. This study provides novel insights into the roles that lncRNAs play in the host response to acute viral infection and paves the way for future lncRNA studies at single-cell resolution.

2022 ◽  
Vol 12 ◽  
Nanxin Liu ◽  
Xiaoxiao Pang ◽  
Hua Zhang ◽  
Ping Ji

Cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) (cGAMP) synthase (cGAS), along with the adaptor stimulator of interferon genes (STING), are crucial components of the innate immune system, and their study has become a research hotspot in recent years. Many biochemical and structural studies that have collectively elucidated the mechanism of activation of the cGAS-STING pathway with atomic resolution have provided insights into the roles of the cGAS-STING pathway in innate immunity and clues to the origin and evolution of the modern cGAS-STING signaling pathway. The cGAS-STING pathway has been identified to protect the host against viral infection. After detecting viral dsDNA, cGAS synthesizes a second messenger to activate STING, eliciting antiviral immune responses by promoting the expression of interferons (IFNs) and hundreds of IFN-stimulated genes (ISGs). Recently, the cGAS-STING pathway has also been found to be involved in response to bacterial infections, including bacterial pneumonia, melioidosis, tuberculosis, and sepsis. However, compared with its functions in viral infection, the cGAS-STING signaling pathway in bacterial infection is more complex and diverse since the protective and detrimental effects of type I IFN (IFN-I) on the host depend on the bacterial species and infection mode. Besides, STING activation can also affect infection prognosis through other mechanisms in different bacterial infections, independent of the IFN-I response. Interestingly, the core protein components of the mammalian cGAS-STING signaling pathway have been found in the bacterial defense system, suggesting that this widespread signaling pathway may have originated in bacteria. Here, we review recent findings related to the structures of major molecules involved in the cGAS-STING pathway and the effects of the cGAS-STING pathway in various bacterial infections and bacterial immunity, which may pave the way for the development of new antibacterial drugs that specifically kill bacteria without harmful effects on the host.

2022 ◽  
Vol 23 (2) ◽  
pp. 815
Soudeh Ghafouri-Fard ◽  
Bashdar Mahmud Hussen ◽  
Hazha Hadayat Jamal ◽  
Mohammad Taheri ◽  
Guive Sharifi

Non-coding RNAs, particularly lncRNAs and miRNAs, have recently been shown to regulate different steps in viral infections and induction of immune responses against viruses. Expressions of several host and viral lncRNAs have been found to be altered during viral infection. These lncRNAs can exert antiviral function via inhibition of viral infection or stimulation of antiviral immune response. Some other lncRNAs can promote viral replication or suppress antiviral responses. The current review summarizes the interaction between ncRNAs and herpes simplex virus, cytomegalovirus, and Epstein–Barr infections. The data presented in this review helps identify viral-related regulators and proposes novel strategies for the prevention and treatment of viral infection.

Mahmoud F. Dondeti ◽  
Mohamed S. Abdelkhalek ◽  
Hosam M El-Din Elezawy ◽  
Walaa F. Alsanie ◽  
Bassem M. Raafat ◽  

2022 ◽  
Vol 19 (1) ◽  
Yuan Chao Xue ◽  
Huitao Liu ◽  
Yasir Mohamud ◽  
Amirhossein Bahreyni ◽  
Jingchun Zhang ◽  

Abstract Background Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of the motor neuron system associated with both genetic and environmental risk factors. Infection with enteroviruses, including poliovirus and coxsackievirus, such as coxsackievirus B3 (CVB3), has been proposed as a possible causal/risk factor for ALS due to the evidence that enteroviruses can target motor neurons and establish a persistent infection in the central nervous system (CNS), and recent findings that enteroviral infection-induced molecular and pathological phenotypes closely resemble ALS. However, a causal relationship has not yet been affirmed. Methods Wild-type C57BL/6J and G85R mutant superoxide dismutase 1 (SOD1G85R) ALS mice were intracerebroventricularly infected with a sublethal dose of CVB3 or sham-infected. For a subset of mice, ribavirin (a broad-spectrum anti-RNA viral drug) was given subcutaneously during the acute or chronic stage of infection. Following viral infection, general activity and survival were monitored daily for up to week 60. Starting at week 20 post-infection (PI), motor functions were measured weekly. Mouse brains and/or spinal cords were harvested at day 10, week 20 and week 60 PI for histopathological evaluation of neurotoxicity, immunohistochemical staining of viral protein, neuroinflammatory/immune and ALS pathology markers, and NanoString and RT-qPCR analysis of inflammatory gene expression. Results We found that sublethal infection (mimicking chronic infection) of SOD1G85R ALS mice with CVB3 resulted in early onset and progressive motor dysfunction, and shortened lifespan, while similar viral infection in C57BL/6J, the background strain of SOD1G85R mice, did not significantly affect motor function and mortality as compared to mock infection within the timeframe of the current study (60 weeks PI). Furthermore, we showed that CVB3 infection led to a significant increase in proinflammatory gene expression and immune cell infiltration and induced ALS-related pathologies (i.e., TAR DNA-binding protein 43 (TDP-43) pathology and neuronal damage) in the CNS of both SOD1G85R and C57BL/6J mice. Finally, we discovered that early (day 1) but not late (day 15) administration of ribavirin could rescue ALS-like neuropathology and symptoms induced by CVB3 infection. Conclusions Our study identifies a new risk factor that contributes to early onset and accelerated progression of ALS and offers opportunities for the development of novel targeted therapies.

2022 ◽  
Jucier Gonçalves Júnior ◽  
Marília de Oliveira Bringel ◽  
Leonardo Rodrigues de Morais ◽  
Luiz Fernando de Castro Malinverno ◽  
Giselle Vasconcelos Liberato ◽  

Although the most common Chikungunya (do not capitalize the disease unless it is named after a proper noun such as Zika, Ebola or Carrion’s Disease) manifestations are osteoarticular, those which bring the most morbidity and mortality are neurological, where thorough mapping through studies with a methodological outline have not yet been well structured. Therefore, the objective was to review the literature to identify neurological manifestations of CHIKV. We used the Virtual Health Library (VHL) and PubMed with the following descriptors: #1 “Chikungunya” [MeSH]; #2 “neurological manifestations” [MeSH] and their equivalents in the Portuguese language, selecting literature published between July 2007 to January 2018. From the 180 studies that were found, 30 were selected. Findings were divided into two subcategories: “Chikungunya: Typical Neurological Manifestations” and “Chikungunya: Severe Neurological Manifestations”. The studies show that headaches were characterized as the most common symptom in adult patients affected by CHIKV, followed by meningeal involvement. Meningeal involvement is also a more serious clinical scenario associated with encephalitis, convulsions, polyneuropathies such as Guillain-Barré syndrome and death. CHIKV is a public health problem for many reasons including its chronic potential complications. Given the neurological symptoms, this disease is concerning in age extremes, for patients with comorbidities and for patients with more than one viral infection by arboviruses, in whom the most severe neurological manifestations are more common.

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