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Vaginal Immunology
Published in William J. Ledger, Steven S. Witkin, Vulvovaginal Infections, 2017
William J. Ledger, Steven S. Witkin
Components of innate immunity also are present within the cytoplasm. A protein kinase known as PKR is activated by double-stranded RNA, an intermediate produced during intracellular viral infections. Activated PKR blocks viral protein synthesis and induces production of the antiviral protein, interferon alpha.
Emergence and Pathogenesis of Avian Influenza in Humans
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Jennifer R. Plourde, Kevin S. Harrod
A well-studied feature of influenza viruses is the ability of the NS1 protein to interfere with the RIG-I pathway.154–156 Specifically, it has been shown that NS1 inhibits tripartite motif 25 (TRIM25) in the ubiquitination of RIG-I, a critical step for type I IFN responses.157 In addition to blocking the production of type I IFNs, NS1 can also bind to the antiviral protein kinase R (PKR). This binding inhibits PKR from down-regulating viral mRNA translation.158
Bunyaviruses
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Patrik Kilian, Vlasta Danielová, Daniel Růžek
The accumulation of viral proteins, maturation and budding of viral particles leads to Golgi apparatus fragmentation and a breakdown of the cell secretory pathway (Salanueva et al. 2003). These processes result in cell death. However, in mosquito cells the situation is completely different. Here, the massive synthesis of viral proteins in the primary phase is followed by a recession, and the infection goes into a persistent phase (Scallan and Elliott 1992). During the primary phase of the infection in mosquito cells in vitro, the cells become highly mobile and form projections that connect to other cells. Structures such as microtubules, mitochondria, GA, and lysozymes can be seen in the projections. The viral nonstructural protein NSm was also observed inside these structures. However, it seems that NSm does not enter uninfected cells via the projections. The most probable function of the structures is to deliver warning signals to uninfected cells. Generally, the formation of complexes consisting of N and L viral proteins is considered to be the first phase of persistent infection (López-Montero and Risco 2011). A similar situation can be observed in mammalian cells when the interferon-induced antiviral protein MxA combines with viral protein N and formed complexes are accumulated in the perinuclear area. Since N protein is required for viral replication, its aggregation limits its utilization for viral multiplication (Kochs et al. 2002). Nevertheless, similar proteins that are responsible for the aggregation of L and N proteins in mosquito cells have not yet been identified.
Oncolytic adenovirus with MUC16-BiTE shows enhanced antitumor immune response by reversing the tumor microenvironment in PDX model of ovarian cancer
Published in OncoImmunology, 2022
Qiuman Wang, Xinyue Ma, Huan Wu, Chen Zhao, Jingying Chen, Rongrong Li, Shi Yan, Yingwei Li, Qing Zhang, Kun Song, Cunzhong Yuan, Beihua Kong
Next, we evaluated the impact of OAd-MUC16-BiTE on the TME using iTRAQ quantitative proteomics and Luminex liquid suspension chip detection. A total of 433 DEPs were screened, of which 261 were upregulated and 172 were downregulated (Figure 6(c)). After OAd-MUC16-BiTE treatment, significant antiviral protein expression was detected, although MAVS protein expression was downregulated (Figure 6(d)). It is worth noting that the expression of proteins related to the promoting T cell migration into tumor tissues (Figure 6(e)) and the processing and presentation of MHC class I antigens (Figure 6(f)) were both upregulated. Consistently, we detected an increase in chemokine levels in tumor tissues treated with OAd-MUC16-BiTE and T cells (Figure 6(h)). Decreased VEGF and basic FGF levels (Figure 6(h)) and increased chemokine levels promote T cell migration into tumor tissues. There is an increase in the concentration of pro-inflammatory factors IL-2, TNF-α, IL-5, IL-6, IL-17A, and IL-9, and a decrease in that of anti-inflammatory factors IL-1.Ra, IL-10, and IL-13, although not significant (Figure 6(i)). In addition, changes in proteins related to T cells function and platinum resistance were also observed (Figure 6(g)).
Quadruple therapy for asymptomatic COVID-19 infection patients
Published in Expert Review of Anti-infective Therapy, 2020
Ling Wang, Xiaopeng Xu, Junshan Ruan, Saijin Lin, Jinhua Jiang, Hong Ye
The two patients in this paper also used hemagglutinin inhibitor, arbidol, which is not recommended by the National Health Commission of China for COVID-19. Arbidol can specifically inhibit the contact, adhesion, and fusion of virus lipid membrane and host cell membrane and block virus gene from penetrating into nucleus, by activating 2,5-oligoadenylate synthetase (antiviral protein) [24,25]. At present, there is no clinical report of arbidol on coronavirus pneumonia, but it has a good inhibition effect on SARS, even Ebola virus (EBOV) and Lassa virus (LASV) in vitro [26–28]. An arbidol concentration of 20 μg/mL was required to achieve a 50% reduction in virus proliferation and hemagglutinin levels [29]. According to China News, cell experiments in vitro showed that arbidol can effectively inhibit COVID-19 up to 60 times at the concentration of 10–30 μM and significantly suppress the pathological effect of the virus on cells [30]. However, the concentration of 10–30 μM is equivalent to 5.3–16.0 µg/mL of arbidol, which is far above the peak concentration (0.41 μg/mL) that can be achieved in vivo by oral administration of single- and multiple-dose arbidol [31,32]. Therefore, whether to apply a higher dose of arbidol for COVID-19 pneumonia needs to be concerned and studied.
Genetic and epigenetic regulation of natural resistance to HIV-1 infection: new approaches to unveil the HESN secret
Published in Expert Review of Clinical Immunology, 2020
Claudio Fenizia, Irma Saulle, Mario Clerici, Mara Biasin
The biological reason for the loss of a potent antiviral protein should result in protection from viral infections is puzzling. Several studies suggest that INFL4 acts as a potent antagonist or a desensitizing factor of IFNA in vivo [82,90–92]. In particular, Obajemu et al. reported that, following viral stimulation, IFN-λ4 induces a particularly prompt and potent production of antiviral ISGs, but stimulates the generation of negative regulators of the IFN response, including USP18 and SOCS1, as well [90]. Therefore, they speculate that the earlier antiviral response endorsed by Type III IFNs can be harmful if it is unproductive and weakens the activity of other IFNs [93], or if it inhibits the acquired immune response [94]. Prompt antiviral release of IFN-λ4 might thus be useful for infections needing an extremely fast, although transitory, immune response, but it is a hazard in infections requiring a more protracted defense such as HCV or HIV. Notably, these studies showed a recessive model of inheritance for the minor alleles in the case of parenteral transmission [87], but a dominant model in the case of sexual transmission and HCV infection [80,88,95,96]. These discrepancies further underline the need to replicate such researches on larger cohorts with different exposure route as different HIV-1 infection risk could correlate with the need of different IFNL4 levels.