Second Virus

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Virus Genome

As more and more bodies are crammed into the unsanitary conditions, the health risks will increase. This refusal to protect those held in detention centers from the spread of infection has caused a bit of an outcry on Twitter with many people comparing it to giving out smallpox infected blankets :. Next Stephen Miller will deliver blankets infected with smallpox. Anne Frank died of typhus. Medical neglect is a genocidal tactic. The CBP claims that they now have more medical personnel than ever before totaling around healthcare workers, but with conditions that include people being crammed into a facility meant for only , the potential for a devastating infection outbreak is very high.

More at CNBC. Although the U. Nowak told a news briefing ,. I would call it inhuman treatment for both the parents and the children. Virus as Composition, Complexity, Quasispecies, Dynamics, and Biological Implications, Second Edition, explains the fundamental concepts surrounding viruses as complex populations during replication in infected hosts.

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Fundamental phenomena in virus behavior, such as adaptation to changing environments, capacity to produce disease, and the probability to be transmitted or respond to treatment all depend on virus population numbers. Concepts such as quasispecies dynamics, mutations rates, viral fitness, the effect of bottleneck events, population numbers in virus transmission and disease emergence, and new antiviral strategies are included. The book's main concepts are framed by recent observations on general virus diversity derived from metagenomic studies and current views on the origin and role of viruses in the evolution of the biosphere.

Grad students, researchers, med students and investigators in virology, microbiology, and infectious disease; pharmacologists and vaccinologists; theoretical biologists; evolutionary biologists. His main interests are the quasispecies structure of RNA viruses and the development of new antiviral strategies. We are always looking for ways to improve customer experience on Elsevier.

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View on ScienceDirect. The herpes simplex virus virion host shutoff vhs RNase destabilizes cellular and viral mRNAs and blunts host innate antiviral responses. Thus, vhs limits accumulation of dsRNA at least in part by reducing the levels of complementary viral transcripts. We then asked if vhs also destabilizes dsRNA after its initial formation. Strikingly, vhs delivered by super-infecting HSV virions accelerates the decay of these pre-formed dsRNAs in both the presence and absence of US11, a novel and unanticipated activity of vhs. Our results show that a herpesvirus host shutoff RNase destabilizes dsRNA in addition to targeting partially complementary viral mRNAs, raising the possibility that the mRNA destabilizing proteins of other viral pathogens dampen the host response to dsRNA through similar mechanisms.

Host organisms therefore deploy a variety of dsRNA receptors to trigger innate antiviral defenses. Not surprisingly, viruses in turn produce an array of antagonists to block this host response. Other less studied viral antagonists appear to function by reducing the levels of dsRNA in infected cells, but exactly how they do so remains unknown.

Here we show that one such viral antagonist, the herpes simplex virus vhs ribonuclease, reduces dsRNA levels in two distinct ways. First, as previously suggested, it dampens the accumulation of partially complementary viral mRNAs, reducing the potential for generating dsRNA. Second, it helps remove dsRNA after its formation, a novel and surprising activity of a protein best known for its activity on single-stranded mRNA.


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Many other viral pathogens produce proteins that target mRNAs for rapid destruction, and it will be important to determine if these also limit host dsRNA responses in similar ways. PLoS Pathog 15 10 : e This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the manuscript and its Supporting Information files. The funders had no role in study design, data collection, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist.

Many if not all viruses produce double-stranded RNA dsRNA as an integral part of their life cycles: RNA viruses must generate complementary RNA species in order to replicate their genome, while DNA viruses produce complementary transcripts from overlapping diverging and converging transcription units. Host cells consequently deploy a variety of pattern recognition PRRs receptors to detect dsRNA and trigger innate antiviral responses, including the type I interferon system [ 1 ].

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Essentially every mammalian virus therefore encodes one or more PKR antagonists, which are required for efficient virus replication in cultured cells and virulence in the intact animal host [ 3 ]. Vhs is packaged into the virion tegument the space between the viral capsid and envelope and delivered into host cells immediately upon infection. Vhs globally destabilizes host mRNAs, thereby suppressing host antiviral responses that require new protein synthesis.

Vhs also destabilizes viral mRNAs [ 27 ], facilitating the successive transitions between the immediate-early IE , early E , and late L phases of viral gene expression by strongly coupling changes in the transcription rates of viral genes to rapidly altered mRNA levels [ 26 — 28 ]. In contrast, vhs has relatively little effect on the levels of viral L transcripts, at least in part because vhs RNase activity is downregulated late during infection through interactions between vhs and additional viral proteins including VP16, UL47, and VP22 [ 29 — 32 ].

In addition to shutting off host protein synthesis and downregulating viral IE and E gene expression at late times post-infection, vhs blunts host innate antiviral and stress responses [ 13 , 14 , 33 — 37 ], and stimulates the expression of viral L genes [ 36 ]. Although deleting vhs has little impact in some cell lines such as Vero cells, viral replication is reduced ca.

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In such restrictive cells, vhs null mutants trigger robust PKR activation [ 13 , 38 ] and formation of stress granules SG, [ 36 , 37 , 39 ] ; in addition, translation of viral true late L2 mRNAs is severely impaired at the level of initiation [ 36 , 40 ]. The ability of vhs to suppress PKR and cellular stress responses and stimulate viral protein synthesis is shared by the mRNA destabilizing proteins of other viruses, illustrating important commonalities between the regulatory strategies of diverse viral pathogens see for example [ 19 , 20 , 41 — 44 ].

Based on the known properties of vhs, at least three distinct mechanisms of PKR suppression can be envisioned, which are not mutually exclusive. Second, vhs is required for efficient expression of US11 an L2 protein in restrictive cell lines [ 36 ], perhaps accounting for some or all of its inhibitory effects on PKR in such cells. Third, vhs might somehow limit the accumulation of dsRNA in infected cells, perhaps through its nuclease activity [ 13 , 35 ]. This hypothesis is plausible and has been broadly accepted in the field, but it has not been directly tested.

Consistent with the proposal, Burgess and Mohr [ 47 ] found that cells infected with vhs-null HSV display enhanced reactivity with a dsRNA-specific monoclonal antibody J2,[ 48 ] in an immunofluorescence assay. However, as we describe below, US11 can shield dsRNA from the J2 mAb in such assays, potentially complicating the interpretation of the results. Here we delineate the roles of vhs and US11 in PKR suppression during infection of permissive and restrictive human cells, and provide direct evidence that vhs limits the accumulation of dsRNA, including species arising from complementary viral transcripts.

These findings significantly advance our understanding of how a viral shutoff ribonuclease dampens host RNA-based innate immune responses, findings that are likely relevant to other viral pathogens that encode RNA destabilizing proteins. As reviewed in the Introduction, vhs has been proposed to limit PKR activation at least in part by reducing the amount of dsRNA in infected cells; however, the levels of dsRNA during infection with wild-type and vhs-null HSV have not been directly measured.

While the nature of the endogenous dsRNA was not determined, it is likely derived in part from transcripts bearing inverted Alu SINE elements [ 49 , 50 ]. Overall, these data indicate that vhs acts directly or indirectly to lower the levels of dsRNA in both cell lines. Although these experiments do not address the origin of the dsRNAs that accumulate in the absence of vhs, we demonstrate below that at least some arise from the viral genome, a finding that is consistent with the observation that PKR activation by Vhs- virus is blocked by inhibiting viral DNA replication and hence the accumulation of viral L transcripts Vhs is required for efficient accumulation of US11 and other HSV true L proteins in some cell lines but not others [ 36 ].

This difference allowed us to uncouple the effects of vhs on US11 levels from its impact on PKR activation. Little effect was observed on expression of ICP These results indicate that vhs and US11 make independent contributions to PKR suppression in these cells, and that when both are missing PKR is hyperactivated and expression of viral L genes is impaired. A slightly different picture emerged in HeLa cells, where US11 expression depends heavily on vhs [ 36 ].

Here as well, deleting vhs or US11 provoked elevated levels of PKR activation, but deleting US11 in the vhs- background had relatively little effect beyond that achieved by inactivating vhs alone, likely because Vhs - is already largely USdeficient in these cells. Overall, these data indicate that vhs and US11 make independent and complementary contributions to PKR suppression when expressed at physiological levels during infection; that is, both proteins are required to fully suppress PKR activity.

A Whole-cell lysates were analyzed by Western blot with the indicated antibodies.

Virus as Populations - 2nd Edition

Note that the Vhs antibody used cross-reacts with a co-migrating cellular protein present in HFF cells. Data are from 4 independent experiments. More recent next generation long-read RNA sequence analysis has confirmed these findings and provided a more detailed picture of the multiple UL23 and ULrelated transcripts arising from this region of the viral genome [ 61 ], summarized in Fig 3A. The probes used for northern blots analysis are diagrammed. Coordinates are from the HSV-1 strain 17 reference genome X Results shown are representative of 3 independent experiments.

The experiment was performed as in E but with a probe specific for the predicted overlap between UL30 and UL31 transcripts. Results shown in E and F are representative of 4 independent experiments each. Thus, vhs dampens the accumulation of the partially complementary UL23 and UL24 RNAs at late times post-infection, limiting the potential for formation of dsRNA in the region of overlap.

To determine if such dsRNA indeed accumulates in the absence of vhs, we treated the purified RNA with the single strand-specific RNases A and T1, then analyzed the resistant material by northern blot using a probe derived from the region of complementarity depicted in red in Fig 3A. One of these band 1 is approximately the length of the known region of complementarity ca.

However, a caveat of the latter conclusion is that these experiments do not exclude the possibility that significant levels of RNA annealing occur during the RNA extraction process.


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Direct evidence that this is not the case under our experimental conditions is presented below Fig 4. A Schematic of dsRNA generation. Transfected cells were treated with actinomycin D for 0, 2 or 4 hours prior to RNA extraction and processed as in B. After 20 hours cells were treated with actinomycinD for 4 hours.

Whole-cell lysates were analyzed by Western blot with the indicated antibodies.