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1 y protect the inhibitor from excision by the viral 3'-5' exonuclease activity.
2 ) chemokine profiles modulated by persisting viral Ags exhibit both discrete functional deficits and
3 ve T cells against at least 1 of 12 analyzed viral Ags, and all patients had Spike-specific T cells.
4 -Cas prokaryotic immune systems provide anti-viral and anti-plasmid immunity via a dual mechanism of
5 n most prominent in the early phase of acute viral and bacterial infections and a molecularly distinc
6 nd Haemophilus influenzae in 14%, and both a viral and bacterial target in 4% of samples.
7        Disentangling the effects of m(6)A on viral and host RNAs remains a challenge for the field.
8        Despite the widespread application of viral- and non-viral-mediated gene transfer to liver, he
9  we describe a strategy utilizing pan-family viral assays to improve early accessibility of large-sca
10 , scalable, and readily deployable surrogate viral assays to screen antiviral humoral responses, defi
11                          Moreover, levels of viral attachment factors and ZIKV are significantly incr
12 nally ablated using either floxed Th mice or viral-based CRISPR/Cas9.
13 division, endosomal vesicle trafficking, and viral budding.
14  viruses and in the production of artificial viral cages for bio/nanotechnological applications.
15 cines showed increase survival for all three viral challenges compared to the wild-type H2 vaccines.
16 unique, large group of light-gated channels (viral channelrhodopsins, VirChR1s).
17 ing episodes during chronic HSV-2 infection; viral clearance always predominated within 24 hours of d
18 es the CD8 T cell response, preventing early viral clearance and immunopathology associated with CD8
19 owards the healthy ecostate, coinciding with viral clearance and recovery.
20 and the relationship to disease severity and viral clearance in COVID-19 patients.
21 of HRCT scores for both disease severity and viral clearance, a standardised HRCT score system for CO
22 SARS-CoV-2 RT-PCR-negative PUIs (n = 30) and viral coinfections in SARS-CoV-2 RT-PCR-positive PUIs (n
23 d to be an important component of the marine viral communities.
24 ing system can generate predictions for each viral component, as well as infer and predict their cont
25 inal microbiota comprises diverse fungal and viral components, in addition to bacteria.
26 -dependent RNA polymerase (RdRP) outside the viral context (RdRP mice) exhibit constitutive, MDA5-dep
27  the main features associated with sustained viral control after ATI in SIV-infected RMs.IMPORTANCE W
28 reviously described an exceptional period of viral control that occurs in some chronically infected w
29 ity to infection, early pathogenesis, innate viral control, adaptive immune responses or the balance
30  which potentially may associate with future viral control.
31 sociated proteins, together constituting the viral core.
32 od donors with acute HIV-1 infection and one viral culture supernatant were serially diluted into 25-
33       SARS-CoV-2 was detected by RT-qPCR and viral culture; the limit of detection for culturing SARS
34 ntly allowed the generation of cKOs by local viral delivery of the Cre-recombinase enzyme.
35                     Lower oxygen saturation, viral detection, and comorbidities were negatively assoc
36 ted protrusion in the envelope V3 loop, this viral determinant does not directly influence V3 loop bn
37 ty of multiple human cell lines to highlight viral determinants that could contribute to H5N1 virus p
38 ible could improve assessment of severity of viral disease in the population.
39  that the use of these agents may facilitate viral disease; thus, they should not be used in high-ris
40 that precluded the generation of viremia and viral dissemination to peripheral organs.
41 ed enzyme kinetic parameters of cellular and viral DNA and RNA polymerases with respect to cellular l
42 equired to maintain full Pol II occupancy on viral DNA and to promote elongation on late genes later
43                                              Viral DNA breakpoints were nonrandom and tended to assem
44 tment with a Pyk2 kinase inhibitor increased viral DNA content in keratinocytes that maintain viral e
45                However, SP-2509 does inhibit viral DNA replication, late gene expression, and virus p
46             Finally, we used an intersecting viral DREADD (designer receptor exclusively activated by
47 ng of syndecan-1 by MMP-3 and MMP-7 supports viral egress.
48 study reveals complex roles of antibodies in viral entry and can guide future vaccine design and anti
49 potential tropism by surveying expression of viral entry-associated genes in single-cell RNA-sequenci
50  O-glycan elaboration also partially blocked viral entry.
51 l DNA content in keratinocytes that maintain viral episomes.
52 As stimulate HLA presentation, which may aid viral evasion of innate immunity.IMPORTANCE Human leukoc
53 A3G activity shapes viral fitness and drives viral evolution in the plasma compartment in humanized m
54 responses play a role in driving early HIV-1 viral evolution.IMPORTANCE HIV-1 has exceptionally high
55  electrostatic charge with immune escape and viral evolutionary dynamics.
56                                Additionally, viral factors such as the HIV-1 accessory protein Nef ca
57                        Importantly, host and viral factors that selectively affect the gammaherpesvir
58 ows that suboptimal anti-A3G activity shapes viral fitness and drives viral evolution in the plasma c
59 he L-IGR (rTCRV/Delta39) exhibited decreased viral fitness in cultured cells, suggesting the feasibil
60 r how size affects the primary components of viral fitness.
61 chronized and controlled, and reconstituting viral fusion to synthetic membranes, which introduces no
62           These studies demonstrate that non-viral gene delivery is impacted by proteoglycan interact
63 e will discuss the recent discoveries on non-viral gene delivery systems.
64                       We demonstrate a novel viral gene expression strategy to target cells with spec
65 erpes simplex virus 1 (HSV-1), can derepress viral genes by degrading ND10 organizers to disrupt ND10
66 otein complex (vRNP) consisting of a dimeric viral genome and associated proteins, together constitut
67 w that KSHV-infected BECs progressively lose viral genome as they proliferate.
68 ata suggest that the epigenetic state of the viral genome is an important determinant of reactivation
69 stein-Barr virus (EBV) switches between four viral genome latency and lytic programmes to navigate th
70  RNA polymerase II transcribing the circular viral genome more than once.
71 enge, and limited inflammation or detectable viral genome or antigen was noted in lungs of animals in
72 d recombinant protein systems to investigate viral genome replication, RNA-binding affinity, ATP hydr
73                                              Viral genome sequencing showed that the majority of HCWs
74  compensatory mutations occurring across the viral genome.
75            This revealed 44,652 high-quality viral genomes (that is, >90% complete), although the vas
76  utility of our method by amplifying partial viral genomes from 6 HeV-infected tissue samples from Sy
77               Sequencing of 1,314 SARS-CoV-2 viral genomes from available patient samples enabled us
78 which highlights the challenge of assembling viral genomes from short-read metagenomes.
79  sequences with a large database of complete viral genomes, including 76,262 identified from a system
80 t the ectodomains of influenza, HIV, and RSV viral glycoprotein trimers.
81  predict which mutations are selected during viral growth in the presence of single antibodies.
82 rval: [18%, 62%]), and a 11% decrease of the viral growth rate (95% credible interval: [4%, 20%]).
83 rvable viremia after a period of exponential viral growth.
84 ARP1 promotes IAV replication by controlling viral HA-induced degradation of host type I IFN receptor
85 ection provides a powerful tool for studying viral-host interactions that should facilitate the disco
86 es to IFN-I restriction, and genetic loss of viral IFN-I antagonists leads to virus attenuation.
87  in cytoplasmic membranous organelles called viral inclusions (VIs) where progeny virions are assembl
88 .51; 95% CI = 4.37-12.91), respiratory tract viral infection (OR = 7.75; 95% CI = 1.60-37.57), cytome
89  fibrils, known as semen-derived enhancer of viral infection (SEVI), that enhance the viral infectivi
90 recognition and binding is the first step of viral infection and a key determinant of host specificit
91  region (MPER) results in robust blocking of viral infection by a class of broadly neutralizing antib
92 late innate and adaptive immune responses to viral infection by engaging with receptors on immune cel
93                                              Viral infection can cause organ dysfunction, but its rol
94 s integral for mechanistic insights into the viral infection cycle, very little is known about the lo
95          A mathematical model describing the viral infection dynamics reveals two transmissibility pa
96                               To investigate viral infection history in KD patients, we performed com
97 F) is the most widely distributed tick-borne viral infection in the world.
98                                              Viral infection is one environmental factor that may con
99 regulation of many ISGs, which confers broad viral infection resistance.
100                                              Viral infection underlies a significant share of the glo
101 ultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for
102 protein response (UPR), a common response to viral infection.
103 tor that recognizes double-stranded RNA from viral infection.
104 ting one potential mechanism for more severe viral infection.
105 to mitigate MuPyV-encephalopathy and control viral infection.
106 y component of the innate immune response to viral infection.
107 luenza-like illness and laboratory-confirmed viral infection; clinical respiratory illness had incons
108 universal face masking policy on respiratory viral infections (RVIs) among admitted very-low-birthwei
109 ll receptors (TCRs) are potent therapies for viral infections and cancer.
110 biome differences after chronic versus acute viral infections and identify CD8 T cell responses and d
111 of intestinal homeostasis.IMPORTANCE Enteric viral infections are a major cause of gastroenteritis wo
112 NGS to assess the frequencies of alternative viral infections in SARS-CoV-2 RT-PCR-negative PUIs (n =
113                        IFNs, produced during viral infections, induce the expression of hundreds of I
114                                      Besides viral infections, IRF3 is also involved in resistance to
115 g prolonged exposure to Ags, such as chronic viral infections, sustained TCR signaling can result in
116  a vaccine vector for the treatment of other viral infections.
117 can increase susceptibility to bacterial and viral infections.
118  of viral infection (SEVI), that enhance the viral infectivity of human immunodeficiency virus.
119 ic integration mechanisms and the impacts of viral integration.
120 uch as neuronal plasticity, development, and viral invasion.
121                                              Viral IRFs 1, 3, and 4 are known to interact with ubiqui
122  EC1+2 domains of human CDHR3 complexed with viral isolate C15a.
123 yV integration, persistent overexpression of viral large T antigen (TAg), and malignancy, yet little
124  of m(6)A writer METTL3 specifically impacts viral late transcripts by reducing their splicing effici
125                                  By modeling viral lattice assembly and recapitulating oscillations i
126  but also TMV as indicators of reductions in viral levels can be applicable during wastewater treatme
127 hese viruses, we examined key aspects of the viral life cycle in three-dimensional (3-D) human airway
128 lear stage (and perhaps other stages) of the viral life cycle, based on several lines of evidence.
129 cological significance of lysogeny and other viral life strategies in nature(6,8-15).
130    The extraordinary immunogenicity of Qbeta viral-like particles relies, in large part, on their abi
131 .001); DBS samples with corresponding plasma viral load >250 copies/ml had a success rate of 86.8%.
132 ong PHIVs, the mean CD4 % was 34%, 93% had a viral load <=20 copies/mL, and 79% were on a nonnucleosi
133                      The risk of an elevated viral load (>=400 copies/mL) was independently lower amo
134 ontraceptives may increase genital tract HIV viral load (gVL) and sexual transmission risk to male pa
135 rology were analyzed by enzyme-immunoassays; viral load by PCR.
136                                          CMV viral load could be decreased and cleared subsequently i
137 nated within 24 hours of detection even when viral load exceeded 1 x 107 HSV DNA copies, and surges i
138 ng integrase inhibitors rapidly suppress HIV viral load in non-pregnant adults, few published data fr
139 osed partners with no report of CD4 count or viral load in the preceding 12 months were presumed not
140 n (<200 copies per mL) was based on the last viral load in the year preceding elicitation, and viraem
141 novel, accurate and cost-effective tools for viral load monitoring become crucial to allow specific d
142                        Restricting to PLHIV, viral load of >=1000 copies/mL was associated with highe
143 g elicitation, and viraemia was defined as a viral load of 200 copies per mL or more.
144 portion of adolescents who had died or had a viral load of at least 1000 copies per muL after 96 week
145 were female, 81% were orphans, and 47% had a viral load of at least 1000 copies per muL.
146 g 12 months were presumed not to be in care, viral load suppression (<200 copies per mL) was based on
147  68.0% (60.9-75.2) to 93.1% (90.2-96.0), and viral load suppression of those on ART increased from 88
148    South African guidelines recommend repeat viral load testing within 6 months when human immunodefi
149  abortions) were eligible for post-pregnancy viral load trajectory analyses (ie, had at least two vir
150                                              Viral load was quantified in acute-phase serum by real-t
151                                       Plasma viral load was significantly correlated with genotyping
152  only variable significantly associated with viral load was time since onset of symptoms.
153  living with HIV (88% of 1321 with available viral load) were virally suppressed, and 673 HIV-negativ
154 onoclonal antibodies are predicted to reduce viral load, ameliorate symptoms, and prevent hospitaliza
155 as a hemorrhagic fever characterized by high viral load, uncontrolled inflammatory response, dysregul
156 after reactivation and correlated with local viral load.
157 HMGB1 translocation and release, and lowered viral load.
158 sitivity was low did not have detectable HCV viral load/core antigen.
159 V improve pulmonary function and reduce lung viral loads and severe lung pathology.
160 -lambda levels (>90th percentile) had higher viral loads and were more likely to have respiratory sic
161                            Periods of stable viral loads are followed by rapid elimination, which cou
162 rom a NiV-infected African green monkey with viral loads as low as 52 genome copies/mg.
163 y-one achieved SVR(12) , 10 had undetectable viral loads but are not eligible for SVR(12) , and 7 rem
164 nths when human immunodeficiency virus (HIV) viral loads exceed 1,000 copies/mL.
165 ad trajectory analyses (ie, had at least two viral loads in the year after end of pregnancy).
166     Colony loss is due, in part, to the high viral loads of Deformed wing virus (DWV), transmitted by
167 rially diluted into 25-ml samples to nominal viral loads ranging from 39 to <0.5 copies (cp)/ml.
168                                   SARS-CoV-2 viral loads, especially plasma viremia, are associated w
169 gress more slowly to AIDS and maintain lower viral loads, presumably due to increased breadth of pept
170 n KSHV-infected endothelial cells undergoing viral lytic reactivation remain unclear.
171 lved in the synthesis of the N-glycan of the viral major capsid protein in PBCV-1 and establishes tha
172 in latently infected HPCs is reexpression of viral major immediate early (MIE) genes.
173 of IBs also must transition prior to further viral maturation, assembly, and release, implying additi
174                                   Using dual viral-mediated gene transfer of DREADDs, we show that tr
175 the widespread application of viral- and non-viral-mediated gene transfer to liver, heart, skeletal m
176 ion is an effective defense strategy against viral-mediated mortality.
177 nvelopment depends upon interactions between viral membrane proteins and tegument proteins that encru
178 to measure thermostability of GP embedded in viral membranes.
179 of maternal immune activation (MIA) with the viral mimic PolyI:C infection during early gestation.
180 sessment of the potential for EBOV to encode viral miRNAs and provides evidence contrary to the exist
181 g process suggest that the real width of the viral mobility distribution is less than 2%.
182 nized as key regulators of both cellular and viral mRNA function.
183 st transcripts could generate chimeric human-viral mRNAs with coding potential.
184  provide novel insights into the dynamics of viral mutation and evolution.
185  abundant type I IFNs (IFN-I) in response to viral nucleic acids.
186         Interestingly, the expression of the viral nucleoprotein (NP) alone is sufficient for the gen
187 ve splicing upon NF-kappaB activation by the viral oncogene Tax of HTLV-1.
188                               The manner how viral oncoproteins hijack the host cell metabolism to me
189 ral variants that contained mutations in the viral open reading frame 5 (ORF5) protein.
190 ection of cytosolic double-stranded DNA from viral or bacterial infection in mammalian cells, cyclic
191                        The BFPP identified a viral or bacterial target in 117/200 (58.5%) samples, in
192  remain largely understudied with respect to viral origin, transmission and replication strategies of
193 ove overall cardiometabolic health so future viral pandemics confer less threat.
194 everal segments, each packaged in a distinct viral particle.
195 heparanase (HPSE) facilitates the release of viral particles by cleaving HS.
196 tivated during, or shortly after, budding of viral particles from the surface of infected cells.
197 aging is a valuable technique for studies of viral pathogenesis and host responses to infection in vi
198 e a crucial hijacking point for a successful viral pathogenesis.
199 ving arms race between antiviral factors and viral pathogens and provide a new means of targeted atte
200 on basin is home to numerous arthropod-borne viral pathogens that cause febrile disease in humans.
201 ial key mechanism of protection against many viral pathogens, antibodies mediate additional immune fu
202 d where those pathways are targeted by human viral pathogens.
203 formed a comprehensive in silico analysis of viral peptide-MHC class I binding affinity across 145 HL
204 he contribution of cellular proliferation to viral persistence is particularly significant in T(EM) c
205 ensation and cell death, enabling studies of viral plaque formation with single-cell resolution.
206  syncytial virus (RSV) is a leading cause of viral pneumonia and bronchiolitis during the first six m
207 ntified as the causal agent for the pandemic viral pneumonia disease, COVID-19.
208 nia, which requires antibiotic therapy, from viral pneumonia, which does not.
209                                   To examine viral population dynamics in orally infected mice, we pr
210 ection of barcoded viruses, we found diverse viral populations throughout each mouse within the first
211 the first day postinfection, but by 48 h the viral populations were dominated by fewer than three bar
212 y of cGAS-STING evasion enzymes evolved from viral proteases through gain of secondary nuclease activ
213 o assemble in large T gene, small T gene and viral protein 2 gene.
214 airs cellular signaling, indicating that the viral protein dysregulates the HP.
215                                          The viral protein Gag selects full-length HIV-1 RNA from a l
216 osttranslational modification is to render a viral protein with diminished abilities to block host re
217  the involvement of other regions of the Gag viral protein.
218 nducible, leading to increased expression of viral proteins upon reactivation.
219  therapy (cART), CPT31 monotherapy prevented viral rebound after discontinuation of cART.
220 y virus (HIV) infection that increase before viral rebound during analytical treatment interruption (
221 major driver of this phenotype and that both viral replication and transcription are affected.
222  and function can be used as an indicator of viral replication before detectable plasma viremia.
223 hat are essential for multiple phases of the viral replication cycle.
224 ARS-CoV-2 strain, and found that it enhances viral replication in human lung epithelial cells and pri
225 ter activity long after the period of active viral replication in peripheral blood.
226                         RT-qPCR demonstrated viral replication in salmon brains up to 15 days postinj
227 sequelae and some with persistent, low-level viral replication in the CNS.
228 uid of RSV-infected mice, without increasing viral replication in the lung.
229  the HIV-1 LTR promoter and facilitate HIV-1 viral replication in the nucleus.
230                                           No viral replication was detectable in the nose of any of t
231 eated with low-dose IFNs show a reduction in viral replication, suggesting the prophylactic effective
232  and elongation activities and essential for viral replication.
233 elerating RT maturation and interfering with viral replication.
234 ovirus 3CL protease, an enzyme essential for viral replication.
235  non-functional and non-genetically evolving viral reservoir along with an HIV-1-specific immune resp
236 jor challenge due to cellular and anatomical viral reservoirs that are often protected from treatment
237 s, livestock, and wildlife that could act as viral reservoirs.
238  enhanced ability to prevent or treat lethal viral respiratory infection in mice, with increased matu
239                                              Viral respiratory infections are risk factors for cardio
240                                        Thus, viral rhodopsins 1 represent a unique, large group of li
241 ) protein forms a conical lattice around the viral ribonucleoprotein complex (vRNP) consisting of a d
242 tep of HIV-1 reverse transcription, in which viral RNA genome is converted into double-stranded DNA,
243                           IFNgamma decreased viral RNA levels only in dAP7 cells and synergized with
244  lacking E1B55K or E4orf6 display defects in viral RNA processing and protein production, but previou
245 -CoV-2) exhibited similar plaque morphology, viral RNA profile, and replication kinetics.
246  are functionally redundant binding sites in viral RNA.
247  or PML significantly increased the level of viral RNAs without altering the level of cccDNA.
248 the structural landscape of other well-known viral RNAs.
249 oolkit to help maximize our understanding of viral roles in health and disease.
250 d local COVID-19 disease status, the role of viral screening and serological testing, return-to-work
251 Cys, but different from those induced by the viral sensors TLR3 or TLR7-9.
252  = 23) were analyzed for clustering of their viral sequences (genetic distance, <2%).
253                                              Viral sequences from infected individuals were grouped i
254 n, while the transmission of KSHV occurs via viral shedding in saliva.
255 ress this question, we used a combination of viral shRNA and conditional mutation to produce cell-spe
256 (90 days postinfection [dpi]) and quantified viral (SIV gag RNA), synaptic (PSD-95; synaptophysin), a
257      However, whether T cells induced by one viral species cross-react with other related flaviviruse
258 oronavirus disease 2019 (COVID-19), uses the viral spike (S) protein for host cell attachment and ent
259 that both of these regions at the top of the viral spike are immunogenic.
260 epresent a natural immune mechanism limiting viral spread.IMPORTANCE HIV infection modulates the surf
261                The establishment of distinct viral strains and their variable circulation patterns pr
262 proteases involved in the activation of many viral strains remain unidentified.
263  Vpu functions among the genetically diverse viral subtypes that contribute to the HIV-1 pandemic.
264 -lived infected cells, and the time to reach viral suppression below a defined detection threshold.
265 ularly among men, eliminating disparities in viral suppression by gender.
266 ased delivery of ART significantly increased viral suppression compared with clinic-based ART, partic
267 nce is a major threat to achieving long-term viral suppression in HIV-positive individuals.
268 n the hospital and retention in HIV care and viral suppression over a 12-month period.
269 ansgender) and (1) retention in care and (2) viral suppression using 2016 client-level RWHAP Services
270 evaluated 6 individuals with HIV (n = 4 with viral suppression using antiretroviral [ART] therapy; n
271 Non-inferiority of DTG + FTC versus cART for viral suppression was assessed using a stratified Mantel
272 istic needs of people living with HIV beyond viral suppression.
273               Abstinence was associated with viral suppression.
274 utpatient care visits, retention in care and viral suppression.
275 sylation sites can alter other properties of viral surface antigens and virions.
276  of Cys mutations in Env glycoprotein on the viral surface, covalent labeling of the Cys residues usi
277 ngement of ED3 clusters on the dengue (DENV) viral surface.
278  EV-A71 by interacting with their respective viral surfaces (glycoprotein gp120 of HIV and the fivefo
279 onal annotation of mutations observed during viral surveillance.
280                                      So far, viral targets of cellular immunity and factors determini
281 al of 104 individuals had an RT-PCR-positive viral test with a cycle threshold (C(T) ) of <35 or sero
282 2-0.8; P = .01), though collinearity between viral testing and clinical service limited our ability t
283                                              Viral testing on day 0 was associated with lower risk of
284 stically significant reduction (P < 0.05) in viral titer in liver and spleen at day 5 postinfection (
285  cell culture-derived particles (HEVcc) with viral titers between 10(5) and 10(6) FFU/mL.
286 ic advantages and disadvantages, which makes viral tool selection paramount for properly designing an
287 of neural circuits is greatly facilitated by viral tools that spread transsynaptically.
288  In this study, we leverage new mouse lines, viral tools, and molecular markers to better define GPe
289 currently applied anterograde and retrograde viral tracers with practical guidance on experimental us
290 s and improvements of H129-based anterograde viral tracers.IMPORTANCE Anterograde transneuronal trace
291                                        Using viral tracing techniques, we determined that PVN -> NAc
292          Here, we present global analyses of viral transcript levels to further understand the roles
293                 Although both early and late viral transcripts contain m(6)A, depletion of m(6)A writ
294 ides a mechanistic insight into saliva-aided viral transmission and could offer a potential prophylac
295  The top 3 prevalent ARI syndromes included: viral upper respiratory tract infection (47%), pharyngit
296 we have discussed the application of HBPs as viral uptake inhibitors in COVID-19 and explained possib
297           To enable a new generation of anti-viral vaccines, we designed self-assembling protein nano
298 ified that bat cells repeatedly selected for viral variants that contained mutations in the viral ope
299 specific CD8(+) T cell responses elicited by viral-vectored CSP-expressing vaccines effectively targe
300 dified Vaccinia Ankara vectors to generate a viral-vectored vaccine, referred to as Nous-209.

 
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