Hpv virus replication cycle


Ion Cantacuzino Institute Rezumat Acest articol este o trecere in revista a hpv virus replication cycle mai recente date din literatura cu privire la stresul Indus reticulului endoplasmic de catre infectia cu virusul gripal A.

S-a descoperit faptul ca virusul gripal A induce calea inositolului —dependent de enzima 1 IRE1 a raspunsului reticulului endoplasmic ER iar inhibarea activitatii caii metabolice IRE1rezultand intr-o replicare virala redusa. Se poate concluziona ca IRE1 poate fi considerat drept o tinta terapeutica potentiala pentru virusul gripal A. Cuvinte-cheie: virusul gripal A, retucul hpv virus replication cycle ERcalea metabolica IRE1 Abstract This article is a review of most recent literature data on role of endoplasmic reticulum ER stress in influenza A viral infection.

It can be concluded that IRE1 may stand as a potential therapeutic target for influenza A virus. Decreasing viral replication by modulating the host ER stress response is a novel strategy that has important therapeutic implications Keywords:influenza virus A, endoplasmic reticulum,IRE1 pathway Introduction It is well known that Influenza A virus has been causing recurrent pandemics for centuries and continues to be a global health threat with a major economic burden[1].

For example, in the United States, seasonal influenza is estimated to cause 36, deaths andhospitalizations annually. The annual Influenza virus epidemics are estimated to cost Furthermore antigenic shift continues o cause recurrent pandemics with a devastating death toll.

More than 40 million people died during the pandemic outnumbering the death toll of World War 1 [4, 5]. With emergence of strains resistant to pharmacologic therapies, yearly vaccination remains the only available strategy for influenza A virus.

Taking into account the limited ability to produce large amounts of vaccines in a short time period which represents a problem at times of pandemics,further understanding of host cellular mechanisms involved in the pathogenesis of influenza A viral infection and identification of therapeutic targets in pronunciation of papillomavirus host are needed for the development of new treatments less susceptible to resistance.

The recent attention has been focused on endoplasmic reticulum ER stress response, also known as the unfolded protein response UPRis a primitive, evolutionary conserved molecular signaling cascade that has been implicated in multiple biological phenomena including innate immunity and the pathogenesis of certain viral infections. The researchers have investigated the effect of influenza A viral infection on ER stress pathways in lung epithelial cells. Influenza A virus induced ER stress in a pathway-specific manner.

When they have examined the effects of modulating the ER stress response on the virus, they have found that the molecular chaperone tauroursodeoxycholic acid TUDCA significantly inhibits influenza A viral replication. In addition, a specific inhibitor of the IRE1 pathway also blocked viral replication.

Their findings constitute the first evidence that ER stress plays a role in the pathogenesis of influenza A viral infection. Decreasing viral replication by modulating the host ER stress response is a novel strategy that has important therapeutic implications. Therefore further understanding of host cellular mechanisms involved in the pathogenesis of influenza A viral infection cancerul pancreatic identification of therapeutic targets in the host are needed for the development of new treatments less susceptible to hpv virus replication cycle.

The endoplasmic reticulum stress response, also known as the unfolded protein response UPRwas originally discovered as an evolutionary conserved molecular signaling cascade the main function of which is to restore ER homeostasis and protein folding capacity during ER stress.

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Over the last decade, the growing body of knowledge about the UPR revealed a broader range of effects implicating it in multiple other cellular and disease processes including apoptosis, inflammation, and metabolism [6—12]. While ER stress has been shown to be involved in the pathogenesis of other viruses [13], its role in influenza A viral infection is neuroendocrine cancer medscape. The adaptive effects of the UPR can be classified into three categories: 1 increasing protein folding capacity of the ER by transcriptional up-regulation of chaperone proteins, 2 decreasing ER protein load by attenuation of global protein translation, 3 increasing proteasome-mediated degradation of misfolded proteins.

Dis Markers ; Mineral bone disorders MBDs constitute a hallmark of CKD, and alongside cardiovascular complications, they underlie a poor prognosis for these patients.

In addition to its hpv virus replication cycle effects, if ER stress is severe or prolonged, the UPR is also known to mediate apoptotic signals to protect the organism from necrotic cell death and inflammation. The factors that determine the balance between the adaptive versus apoptotic effects are still not well understood [14].

BiP hpv virus replication cycle a major chaperone protein and is considered the master regulator of the UPR hpv virus replication cycle. Cleaved ATF6 functions as a transcription factor for chaperone hpv virus replication cycle. In light of the growing evidence of diverse interactions between viral infections and ER stress the authors have investigated the effects of influenza A viral infection on the different pathways of the UPR and the potential role of ER stress in viral replication.

Over the last decade, several groups of laboratories have reported the induction of ER stress in the setting of some viral infections. However, very little is known about the mechanisms by which ER stress is induced or about the role of the UPR in the pathogenesis of these viruses.

Until recently,the only studies linking influenza infection to ER stress are ones showing that hemagglutinin A induces ER stress. The papilloma virus isterectomia proposed by the investigators was hpv virus replication cycle induction of ER stress but it was not directly proven [16].

The most recent literature data is first evidence that infection with wild type influenza A virus hpv virus replication cycle ER stress. Furthermore the researchers showed that influenza A viral infection induces the ER stress response, in primary human airway epithelial cells, in a pathway- specific manner.

They also showed that the virus modulates the stress response in the setting of a preexisting stress by decreasing the activation of the ATF6 pathway as indicated by its inhibitory effect on ATF6-driven genes. In airway epithelial cells, the effects of a virus on ER stress are different.

Although the mechanism by which influenza A virus induces ER stress could be the accumulation of viral proteins in the ER lumen, the differential effects on the different pathways of the UPR are indicative of additional levels of interaction between the virus and the ER stress signaling cascade.

The mechanism behind differential activation of the different arms of the UPR is unknown [14]. This suggests that the UPR plays a facilitating role in the replication cycle of the virus. The combined effects of influenza A viral infection on the ER stress pathways seem to be aiming at optimal activation of IRE1 pathway.

By inhibiting the ATF6 pathway, the activation of which is known to increase the ER folding capacity hpv virus replication cycle to alleviate the ER stress response, the virus may be sarcoma cancer causes optimal and sustained activation of IRE1.

The inhibition of influenza A viral replication with TUDCA, which alleviates the ER stress response, hpv virus replication cycle that one or more of the downstream effects of IRE1, the only ER stress pathway activated by the virus, is required for viral replication This was confirmed in by the most recent studies studies by the inhibition of viral replication with the use of the IRE1 inhibitor,3,5-dibromosalicylaldehyde.

Conclusion The new data obtained by scientists regarding implication of the UPR in hpv virus replication cycle A viral replication hpv virus replication cycle a novel finding that could lead to new therapies for influenza A virus respiratory infection. By targeting a host cellular mechanism, such therapies are less susceptible to viral resistance mechanisms.

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The scientific interest has been in studying the effects of chemical chaperones, in particular TUDCA, on in vivo models of influenza A viral infection.

They have anticipated the effects to be more complex than merely inhibiting viral replication. The disease manifestations of influenza A viral infection are in part due to the host immune response and inflammatory cytokines [17].

Therefore modulation of the ER stress response by chemical chaperones may cause a change in the cytokine milieu created by the infection and therefore a change in the disease phenotype. Furthermore,MHC class I expression on the cell surface, which is important in antigen presentation and in mediating T hpv virus replication cycle immunity, is dependent on the ER function [].

Improving the ER folding capacity with chemical chaperones may render dendritic cells more efficient in presenting viral antigens and therefore accelerating viral clearance.

The combined effect of all these potential mechanisms is difficult to predict and an area of future study is needed.

  1. Implicarea genomului papiloma virusului uman (hpv) în oncogeneza cancerului cervical
  2. The virus infects basal epithelial cells of stratified squamous epithelium.
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