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1                                              Viral infection can cause organ dysfunction, but its rol
2                                              Viral infection can change the expression patterns of di
3                                              Viral infection is now recognized as a ubiquitous top-do
4                                              Viral infection is one environmental factor that may con
5                                              Viral infection underlies a significant share of the glo
6                                              Viral infections during pregnancy can have devastating c
7                                              Viral infections trigger host innate immune responses, c
8                                              Virus infection of cells lacking DUSP11 results in a hig
9                                   SARS-CoV-2 viral infection triggers various inflammatory, biochemic
10 o exert different functions in vivo during a viral infection, in a manner tightly orchestrated in tim
11 llnesses, leading some to hypothesize that a viral infection is the inciting event for KD.
12            In a disease context, influenza A virus infection impaired AM crawling via the type II int
13 functional characteristics after influenza A virus infection of B6 mice.
14  birth increases the severity of influenza A virus infections in adult mice by reducing the number of
15                                     Abortive viral infections are usually studied in populations of s
16 pulations provide averaged information about viral infections, single-cell analyses offer individual
17  traits that peak and last long after active viral infection is cleared.
18 ing antibody response is typical of an acute viral infection, with declining neutralizing antibody ti
19 ad T cell activation characteristic of acute viral infection and plasmablast responses reaching >30%
20 ost is critical for the restriction of acute viral infections.
21 d immunity after coronavirus and other acute viral infections, we posit that, with few exceptions, th
22  of tissue-specific effects of primary acute viral infections like COVID-19 are essential for underst
23 biome differences after chronic versus acute viral infections and identify CD8 T cell responses and d
24 es to the prevention of severe disease after virus infection include both a paucity of protective vac
25 mune response is crucial for defense against viral infections.
26 resents an ancient defense mechanism against viral infections.
27 s that breast milk can be protective against viral infections(8-10).
28  system is the first line of defense against virus infection.
29 where they provide adaptive immunity against virus infection and plasmid transformation.
30  both coinfections (1, 2.2%) and alternative viral infections (4, 13.3%) that were not detected by ro
31 y, limiting our understanding of alternative viral infections and coinfections in these patients.
32 NGS to assess the frequencies of alternative viral infections in SARS-CoV-2 RT-PCR-negative PUIs (n =
33 n post-operative inflammation, bacterial and viral infection and infection with or without organ dysf
34 es is related to diseases such as cancer and viral infection.
35 c cell immunization, Listeria infection, and viral infection.
36  degradation and interferon suppression, and viral infection under interferon-competent conditions.
37 by increased susceptibility to bacterial and viral infections and (to a lesser extent) autoimmune man
38 deleterious to the host during bacterial and viral infections.
39 can increase susceptibility to bacterial and viral infections.
40 commonly used in the treatment of cancer and viral infections.
41 erge in the development of human cancers and viral infections, but their relevance to bacterial disea
42 ghest for respiratory, gastrointestinal, and viral infections.
43  the relationships between host genetics and viral infections, the contributions of respiratory viral
44 e regulated by T1D genetic risk variants and viral infections associated with T1D.
45                                    IL-13 and virus infection mediated effects on ACE2 expression were
46 nge needed to facilitate membrane fusion and virus infection, and the epitope recognized by h5B3.1 ha
47                                   Antecedent viral infection may contribute to increased susceptibili
48 ancer development and progression as well as viral infection, notably by HIV-1.
49 ty, stimulated by cellular stresses, such as viral infections and ER stress, leads to the regulation
50 , additional environmental triggers, such as viral infections, are usually required to initiate the o
51 IAV-induced splicing pattern also attenuates viral infection.
52 , immunizing populations against hepatitis B virus infection, and screening for colorectal cancer.
53 1; immunology, P = 0.02) but not influenza B virus infection.
54 roved in 2018 for treating influenza A and B virus infections.
55  that NF-kappaB is rendered inactive because virus infection results in reduced levels of upstream in
56                                      Besides viral infections, IRF3 is also involved in resistance to
57                        The interplay between viral infection and Alzheimer's disease (AD) has long be
58  provide a possible mechanistic link between viral infection, bloom termination, and mass carbon expo
59 es that bind the capsid protein VP1 to block viral infection.
60 f new antiviral strategies aimed at blocking viral infection at very early stages.
61 F) is the most widely distributed tick-borne viral infection in the world.
62 regulation of many ISGs, which confers broad viral infection resistance.
63  cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, p
64  1 and 2 IFN signatures, normally induced by viral infections.
65 n, or uncontrolled inflammation triggered by viral infections during pregnancy, and its potential dow
66 IFN-beta are type I IFNs that are induced by virus infection and are important in the host's innate a
67 st innate immunity against hepatitis B and C viral infections by inducing m(6)A modification of viral
68                                  Hepatitis C virus infection (OR, 15.84; 95% confidence interval [CI]
69 hroughout her life, leading to a hepatitis C virus infection (which was treated, achieving a sustaine
70  the burden of disease caused by hepatitis C virus infection is proving difficult, despite the availa
71 pproximately 29.6% prevalence of Hepatitis C virus infection observed among inmates studied is high a
72 Poverty, injection drug use, and hepatitis C virus infection were also associated.
73 sons with chronic hepatitis B or hepatitis C virus infection.
74 n associated with an increase in hepatitis C virus infections among women of childbearing age in the
75 chanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neut
76 ute and chronic lymphocytic choriomeningitis virus infection in the joint and spleen.
77 te that chronic lymphocytic choriomeningitis virus infection rapidly triggers severe thymic depletion
78 -I responses to lymphocytic choriomeningitis virus infection were augmented in newly generated mice l
79                                      Chronic viral infection leads to inflammation and liver damage,
80 and augmented responses to acute and chronic viral infection.
81              However, the effects of chronic viral infection on T-cell responses and vaccination agai
82 g prolonged exposure to Ags, such as chronic viral infections, sustained TCR signaling can result in
83 ing to the clonality observed during chronic viral infections.
84                                   In chronic viral infections, the deranged B cell subset signifies u
85          It is well established that chronic viral infections can cause immune suppression, resulting
86 CE CD8 TCR repertoires responding to chronic viral infections (HIV, hepatitis C virus [HCV], Epstein-
87      Although HCC is associated with chronic viral infections, alcoholic cirrhosis, and nonalcoholic
88 first to define the role of IRF-7 in chronic virus infection.
89 he context of the CNS development, acute CNS viral infections, and post-infectious and noninfectious
90 the development of novel therapies to combat viral infection.
91                                 In combating viral infections, the Fab portion of an antibody could m
92 luenza-like illness and laboratory-confirmed viral infection; clinical respiratory illness had incons
93 to mitigate MuPyV-encephalopathy and control viral infection.
94            Natural killer (NK) cells control viral infection through the interaction between inhibito
95  I interferons are important for controlling virus infection.
96 d to understand the mechanisms to counteract virus infection.
97 eath pathway in cells that successfully cure viral infection.
98  membrane to reach the cytosol is a decisive virus infection step.
99                                       Dengue virus infection also induced cross-reactive MBC response
100 on this association in the context of dengue virus infection (DENV).
101 mpaign were seropositive for previous dengue virus infection.
102 nsmissions in human population and detecting viral infection outbreaks.
103  as blood coagulation, skeletal development, viral infection, cell-cell fusion, and ataxia.
104 he Dispanin/CD225 family and inhibit diverse virus infections.
105 (d p.i.), although both wild-type and DUBmut virus infections resulted in similar liver pathology.
106 in Nfkbia(NES/NES) mice poorly expand during viral infection, and this can be overcome by exogenous I
107 ch with differential response options during viral infection.
108  endogenous cyclic GMP-AMP signalling during viral infection and anti-tumour immunity(1-5).
109 sence of glycolipid Ags, for example, during viral infections.
110                        IFNs, produced during viral infections, induce the expression of hundreds of I
111 s to mount an effective host response during viral infections.
112 at other functions pDCs exert in vivo during viral infections is controversial, and more studies are
113 ts into the way that ANP32A might act during virus infection.IMPORTANCE Successful zoonotic transmiss
114 cs and magnitude of the host response during virus infection and demonstrates that inactivating a dom
115          Recent studies indicate that during virus infection, phloem tissues are a source of signific
116 al ISGs not previously known to affect Ebola virus infection.
117                               In human Ebola virus infection, clinical outcome is strongly associated
118 gents for the treatment and control of Ebola virus infections.
119 y for enteric cytopathic human orphan (echo) virus infection.
120 erefore unlikely to contribute to or enhance viral infection.
121 mary receptor for pathogenic NWAs, enhancing viral infection in guinea pigs.IMPORTANCE JUNV is one of
122 tal roles in immune defenses against enteric viral infections by integrating diverse signals, includi
123 of intestinal homeostasis.IMPORTANCE Enteric viral infections are a major cause of gastroenteritis wo
124  an immunodominant antigen in many enveloped virus infections.
125                                     Epidemic viral infections predominated as causes of childhood enc
126 sional (3-D) human airway tissues to examine viral infection in a physiologically relevant model syst
127  learned from birth cohort studies examining viral infections and subsequent asthma and from understa
128 eins and has a putative role in facilitating viral infection.
129 ctive in the intestinal epithelium following viral infection, but our understanding of the benefits o
130  the host's cell immunity response following virus infection.
131 al changes were observed and no evidence for viral infection or integration could be provided after l
132 ll receptors (TCRs) are potent therapies for viral infections and cancer.
133 in heavy chain-binding motif were needed for virus infection, whereas the inositol phospholipid-bindi
134 ntry into target cells is the first step for virus infection.
135  protein and failed to protect macaques from viral infection.
136 tor that recognizes double-stranded RNA from viral infection.
137 answer outstanding questions regarding giant virus infection mechanisms, we set out to determine biom
138                      We find that 3c2.A H3N2 virus infections boost non-neutralizing H3N2 antibodies
139  more than 850 confirmed human cases of H5N1 virus infection have been reported, of which ~60% were f
140  step and suggest promising routes to hinder viral infections by inducing mis-assembly.
141                       Human immunodeficiency virus infection was also associated with increased risk
142 t drugs used to treat human immunodeficiency virus infection, and their use can cause mitochondrial t
143 ry diseases including human immunodeficiency virus infection, psoriasis, rheumatoid arthritis, and sy
144  by acute simian (or human) immunodeficiency virus infection may persist or spontaneously resolve in
145 ters the cellular environment, which impacts viral infection in immortalized cells.
146 in response to type I interferons.IMPORTANCE Viral infection triggers the secretion of type I interfe
147 orm of the hepatitis B virus (HBV) genome in viral infection and an undisputed antiviral target for a
148 rocesses that impact human health, including viral infections.
149 presence of butyrate, resulting in increased virus infection and replication.
150                          Thus, the increased virus infection in the fetus was not the result of an im
151 nds for the potential treatment of influenza viral infections.IMPORTANCE Influenza viruses are highly
152 athways related to respiratory and influenza virus infection.
153 tory signals during modified avian influenza virus infection.
154  study, index cases with confirmed influenza virus infection and their household contacts were follow
155 ic and resilient microbiome during influenza virus infection in multiple hosts provides a compelling
156 nsing of the Z-RNA produced during influenza virus infection induces cell death in the form of pyropt
157 r impact on T cell motility during influenza virus infection.
158 on inside an artery resulting from influenza virus infection as the primary outcome of this integrate
159 therapeutic application against H1 influenza virus infection in humans.
160       To study the contribution of influenza virus infection to cardiovascular thrombotic events, we
161 e with lung damage and severity of influenza virus infection.
162 vid-19 from that of equally severe influenza virus infection.
163 blood clotting may be connected to influenza virus infection.
164 tudies need to investigate whether influenza virus infection affects susceptibility for aortic dissec
165 ed and antigenically-characterised influenza virus infections from Australia, we investigate the effe
166  the most effective way to prevent influenza virus infections.
167 s first encountered during primary influenza virus infections.
168                           Seasonal influenza virus infections cause mild illness in healthy adults, a
169 boxil, 4, is approved for treating influenza virus infections.
170 and inform therapeutic strategies to inhibit viral infection.
171     A subset of these antibodies can inhibit virus infection, thus making E a suitable candidate for
172 ighting the cells' potential role in initial viral infection, spread and clearance.
173  knowledge of the progression of the initial viral infection is limited, and no safe or effective vac
174 arallel experiments with direct intracranial virus infection generated similar results.
175                               To investigate viral infection history in KD patients, we performed com
176                      However, cases of Junin virus infection, a related virus, can be treated with co
177 attempts to reverse and eliminate the latent viral infection that prevents eradication of the virus.
178 s the individual's ability to control latent viral infections.
179 lic reprogramming of host cells during lytic viral infection alters the flow of energy and nutrients
180 to provide quantitative descriptions of many viral infections, but for the Ebola virus, which require
181 S2 (transmembrane protease serine 2) mediate viral infection of host cells.
182 izes with PS to promote PS receptor-mediated virus infection and clearance of apoptotic cells.
183 , but only partially block DC-SIGNR-mediated virus infection.
184 tibody levels that may protect against mumps virus infection for longer than previously assumed and i
185 vous system (CNS) following many neurotropic virus infections.
186 ent signaling pathways in the attenuation of viral infection and may lead to the development of new a
187 ns of the two pathways to the attenuation of viral infection are different in mouse versus human cell
188  and the TLR3 pathways in the attenuation of viral infection may be species specific.IMPORTANCE The m
189  region (MPER) results in robust blocking of viral infection by a class of broadly neutralizing antib
190 tem of different species under conditions of viral infection, stress, or disease.
191 roles of individual miRNAs in the context of viral infection remain largely uncharacterized.
192 pes of RNA sensed by RLRs in the contexts of viral infection, malignancies and autoimmune diseases.
193  gene expression relevant for the control of viral infection, with both proteins potentially facilita
194 ar distinctions drawn between enhancement of viral infection at the plasma membrane and amphipathicit
195  fibrils, known as semen-derived enhancer of viral infection (SEVI), that enhance the viral infectivi
196 ugh recombinant EC1 is a potent inhibitor of viral infection, there is no molecular description of th
197  in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs.
198 ical regulatory gene, and permit modeling of viral infection.
199     Both ARVs and NAbs prevent new rounds of viral infection, but NAbs may have the additional capaci
200                    One of the first signs of viral infection is body-wide aches and pain.
201 recognition and binding is the first step of viral infection and a key determinant of host specificit
202  organ culture to study the initial steps of viral infection and the consequent innate immune respons
203         We anticipate that future studies of viral infection kinetics with this reporter system will
204 ely reflecting their dual role as targets of viral infection and key components of the host response.
205 on and can be linked to specific outcomes of viral infections.
206 of environmental exposure on the severity of viral infections, and how the viral genome influences ho
207 adaptive immune defense against a variety of viral infections.
208 nd preparing for possible recurrent waves of viral infections.
209 ype III IFN for the control and clearance of virus infection, but the physiological basis of this sel
210 ed epitope-tagged proteins in the context of virus infection in order to detect CHPK in the host.
211 ospheres with IFNs recapitulates features of virus infection, including cell death.
212 -I)-like receptors (RLRs) are key sensors of virus infection, mediating the transcriptional induction
213 lly modified zebrafish to visually report on virus infections.
214 ines that contained galbut virus as the only virus infection and showed that these flies can be used
215 lantation monitoring of common opportunistic viral infections and of graft rejection, and should faci
216 nfavorable conditions (e.g. tumor hypoxia or viral infection), canonical, cap-dependent mRNA translat
217 IPF, which may be caused by bacterial and/or viral infections.
218 r specific to shared background mutations or viral infections.
219 inant Le Blanc delta was able to block Orsay virus infection in worm culture and vice versa, suggesti
220 HIPR-1) as a host factor essential for Orsay virus infection of C. elegans Ablation of HIPR-1 resulte
221 ed for inducing the IPR in response to Orsay virus infection but not in response to other triggers li
222 sting T-cells, SAMHD1 blocks HIV-1 and other viral infections by depletion of the dNTP pool to a leve
223 y also offer therapeutic potential for other viral infections.
224  a vaccine vector for the treatment of other viral infections.
225 the treatment of mammarenavirus and/or other viral infections in humans.
226  the treatment of JUNV and potentially other viral infections.
227  in humans and is prototypic of a persistent viral infection characterized by periods of latency.
228  stem-like subset late during the persistent viral infection.
229  immunotherapeutic approaches for persistent viral infections.FUNDINGDeutsche Forschungsgemeinschaft
230 austed CD8(+) T cell responses in persistent viral infections or tumors.
231 bution to the outcome of acute or persistent viral infections has remained elusive.
232  sphingosine can be also employed to prevent viral infections.
233 monstrate the differential effect of primary viral infections in the susceptibility to disease exacer
234 -producing B cells and suffer from prolonged virus infections.
235 otropic viruses in neuronal cells and rabies virus infection in mouse brains.
236 f orlistat (tetrahydrolipstatin) in reducing virus infection for several mosquito borne viruses inclu
237                                  Respiratory viral infection causes chronic obstructive pulmonary dis
238 mory CD8 T cell formation during respiratory viral infection.
239 context of the treatment of this respiratory viral infection.
240                            Acute respiratory viral infections are a major cause of respiratory morbid
241 ative PCR cutoffs for diagnosing respiratory viral infections.
242 echanisms by which aging impacts respiratory viral infections, including SARS-CoV-2.
243 infections, the contributions of respiratory viral infections to patterns of immune development, the
244 universal face masking policy on respiratory viral infections (RVIs) among admitted very-low-birthwei
245 ease is strongly associated with respiratory viral infections, but the impact of viruses on Streptoco
246  is a recognised complication of respiratory virus infections, increasing morbidity and mortality, bu
247 alized innate immunity component to restrict viral infection.
248    Here, we have shown that upon DNA and RNA viral infection, macrophages reduced 7-dehydrocholestero
249 kably, in response to dsRNA treatment or RNA virus infection, LGP2 is rapidly released from MAVS and
250                                      Second, viral infection depends on the physiological state of th
251 rbation in response to a different secondary viral infection and highlight the usefulness of these vi
252  and TNF-alpha mRNA levels induced by Sendai virus infection.
253 ntial pathogen recognition receptors sensing viral infections while LGP2 has been described as both R
254 ndidate inhibitors were validated in several viral infection assays.
255 ting one potential mechanism for more severe viral infection.
256 terial pigment in controlling herpes simplex virus infection, for which diverse and multimodal antivi
257                98 (49%) of them had a single viral infection (41 [20%] had Zika, 55 [27%] had chikung
258 t of granule-mediated cytotoxicity, specific viral infections, excess IL-18, and chimeric antigen rec
259       YAP slows T cell responses in systemic viral infections and retards effector T cells in autoimm
260               Immunopathogenesis in systemic viral infections can induce a septic state with leaky ca
261                           Here, we show that viral infection with LCMV results in type I IFN-dependen
262 irus (SINV) in Drosophila, here we show that viral infections affect TE transcript amounts via modula
263                                          The viral infection was further confirmed by molecular metho
264 ultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for
265          A mathematical model describing the viral infection dynamics reveals two transmissibility pa
266 s integral for mechanistic insights into the viral infection cycle, very little is known about the lo
267    We performed serological profiling of the viral infection history in 899 individuals from an NCI-U
268                                Following the virus infection, the MEG-01 cells showed a marked reduct
269 ay in the individual immune response to this viral infection.
270  increases the risk of severe disease due to viral infection.
271 ylate (cOA) second messengers in response to viral infection of bacteria and archaea, potentiating an
272 ide contributes to the beta-cell response to viral infection.
273 y component of the innate immune response to viral infection.
274 protein response (UPR), a common response to viral infection.
275 aceted role in the innate immune response to viral infection.
276 e TBK1/IRF3 signaling pathway in response to viral infection.
277  acts to suppress the interferon response to viral infection.
278  generates cyclic nucleotides in response to viral infection.
279 ole in the regulation of the IFN response to viral infection.
280 SAMHD1 suppresses innate immune responses to viral infection and inflammatory stimuli by inhibiting t
281 late innate and adaptive immune responses to viral infection by engaging with receptors on immune cel
282 eletion increases cellular susceptibility to viral infection in vitro, and that Snx5 knockout in mice
283  a genomic record of historical tolerance to viral infection in bats.
284 ic, innate, and adaptive immune responses to viral infections in the respiratory tract.
285 l genome influences host immune responses to viral infections.
286                               In response to virus infection, the acetylated Lys129 is removed by SIR
287 egral roles in the innate immune response to virus infection.
288 d in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D).
289 .51; 95% CI = 4.37-12.91), respiratory tract viral infection (OR = 7.75; 95% CI = 1.60-37.57), cytome
290  prior or concurrent upper respiratory tract viral infection, this bacterium commonly causes multiple
291  Despite global efforts to prevent and treat virus infections to limit morbidity and mortality, the c
292 in mediating antiviral protection in various viral infections, necessitating a detailed understanding
293 als, such AuraShield L, can prevent in vitro viral infection of cell cultures.
294  culture limit the ability to study in vitro virus infection and inhibition in this medium.
295 ial cells and extend our findings to in vivo viral infections.
296   Our work reveals a mechanism through which viral infections cause heightened pain sensitivity.
297 s of environmental contamination but without virus infection.
298                                         Zika virus infection occurred at 16-33 weeks gestation.
299 es during epidemics.IMPORTANCE Although Zika virus infection of pregnant women can result in congenit
300 nt of the neurological complications of Zika virus infection.

 
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