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1 y component of the innate immune response to viral infection.
2 to mitigate MuPyV-encephalopathy and control viral infection.
3 the development of novel therapies to combat viral infection.
4 c cell immunization, Listeria infection, and viral infection.
5 protein response (UPR), a common response to viral infection.
6 mory CD8 T cell formation during respiratory viral infection.
7 eins and has a putative role in facilitating viral infection.
8 ide contributes to the beta-cell response to viral infection.
9 stem-like subset late during the persistent viral infection.
10 and inform therapeutic strategies to inhibit viral infection.
11 ay in the individual immune response to this viral infection.
12 and augmented responses to acute and chronic viral infection.
13 alized innate immunity component to restrict viral infection.
14 eath pathway in cells that successfully cure viral infection.
15 context of the treatment of this respiratory viral infection.
16 aceted role in the innate immune response to viral infection.
17 erefore unlikely to contribute to or enhance viral infection.
18 e TBK1/IRF3 signaling pathway in response to viral infection.
19 es is related to diseases such as cancer and viral infection.
20 tor that recognizes double-stranded RNA from viral infection.
21 ed to handle acute illness after respiratory viral infection.
22 elopmental disorders and hypersensitivity to viral infection.
23 tion, wound healing, cancerous invasion, and viral infection.
24 rive can be used as a strategy to suppress a viral infection.
25 rmitting asthma development after early-life viral infection.
26 verexpressed Prevotella proteins can promote viral infection.
27 xamine complex neurological phenotypes after viral infection.
28 fferences between controls and bacterial and viral infection.
29 such as clonal expansion and memory, during viral infection.
30 endosomes-for initiation of autophagy during viral infection.
31 FI44L can serve as a diagnostic biomarker of viral infection.
32 ng of the processes by which m(6)A regulates viral infection.
33 es that show considerable variability during viral infection.
34 ting one potential mechanism for more severe viral infection.
35 nction with antiviral therapy during chronic viral infection.
36 gulating circulating lymphocyte responses to viral infection.
37 st cofactor that facilitates early stages of viral infection.
38 acts to suppress the interferon response to viral infection.
39 ical regulatory gene, and permit modeling of viral infection.
40 generates cyclic nucleotides in response to viral infection.
41 ole in the regulation of the IFN response to viral infection.
42 es that bind the capsid protein VP1 to block viral infection.
43 increases the risk of severe disease due to viral infection.
44 IAV-induced splicing pattern also attenuates viral infection.
45 ch with differential response options during viral infection.
46 protein and failed to protect macaques from viral infection.
47 a vaccine vector for the treatment of other viral infections.
48 IPF, which may be caused by bacterial and/or viral infections.
49 commonly used in the treatment of cancer and viral infections.
50 mune response is crucial for defense against viral infections.
51 s to mount an effective host response during viral infections.
52 ing to the clonality observed during chronic viral infections.
53 nd preparing for possible recurrent waves of viral infections.
54 s the individual's ability to control latent viral infections.
55 y also offer therapeutic potential for other viral infections.
56 rocesses that impact human health, including viral infections.
57 ost is critical for the restriction of acute viral infections.
58 the treatment of JUNV and potentially other viral infections.
59 can increase susceptibility to bacterial and viral infections.
60 neating guidelines on MAb usages in treating viral infections.
61 ion-based classifier for acute bacterial and viral infections.
62 nce of refractory fungal, mycobacterial, and viral infections.
63 cells are key for immune protection against viral infections.
64 Chronic viral infections.
65 to promote diseases, especially respiratory viral infections.
66 s seen with nucleoside/tide analogs in other viral infections.
67 e diseases or promote IFN-I secretion during viral infections.
68 to prevent, limit, and treat these dangerous viral infections.
69 an important role in this and other emerging viral infections.
70 resents an ancient defense mechanism against viral infections.
71 r specific to shared background mutations or viral infections.
72 sphingosine can be also employed to prevent viral infections.
73 on and can be linked to specific outcomes of viral infections.
74 sence of glycolipid Ags, for example, during viral infections.
75 ial cells and extend our findings to in vivo viral infections.
76 ative PCR cutoffs for diagnosing respiratory viral infections.
77 ghest for respiratory, gastrointestinal, and viral infections.
78 deleterious to the host during bacterial and viral infections.
79 l genome influences host immune responses to viral infections.
80 1 and 2 IFN signatures, normally induced by viral infections.
81 adaptive immune defense against a variety of viral infections.
84 both coinfections (1, 2.2%) and alternative viral infections (4, 13.3%) that were not detected by ro
87 st translation, and tested it in the case of viral infection, a common form of naturally occurring ex
88 rons, one of the first mediators produced by viral infection, act directly on nociceptors to produce
89 irus (SINV) in Drosophila, here we show that viral infections affect TE transcript amounts via modula
92 lic reprogramming of host cells during lytic viral infection alters the flow of energy and nutrients
93 testing algorithms identify most respiratory viral infections among SARS-CoV-2 PUIs, when available a
94 recognition and binding is the first step of viral infection and a key determinant of host specificit
96 orm of the hepatitis B virus (HBV) genome in viral infection and an undisputed antiviral target for a
100 ribing how m(6)A modulates host responses to viral infection and discuss future directions that will
101 ver, the MG-hBORG model supported productive viral infection and exhibited increased inflammatory res
102 rbation in response to a different secondary viral infection and highlight the usefulness of these vi
103 detailed overview of the role of glycans in viral infection and highlights experimental approaches t
104 esults indicated that S411A Kunjin decreased viral infection and increased cytopathogenicity in cell
105 n post-operative inflammation, bacterial and viral infection and infection with or without organ dysf
106 VSV-eGFP-SARS-CoV-2 show profoundly reduced viral infection and inflammation in the lung, indicating
107 SAMHD1 suppresses innate immune responses to viral infection and inflammatory stimuli by inhibiting t
108 ely reflecting their dual role as targets of viral infection and key components of the host response.
110 ent signaling pathways in the attenuation of viral infection and may lead to the development of new a
113 ad T cell activation characteristic of acute viral infection and plasmablast responses reaching >30%
114 organ culture to study the initial steps of viral infection and the consequent innate immune respons
116 by increased susceptibility to bacterial and viral infections and (to a lesser extent) autoimmune man
118 y, limiting our understanding of alternative viral infections and coinfections in these patients.
121 ty, stimulated by cellular stresses, such as viral infections and ER stress, leads to the regulation
122 biome differences after chronic versus acute viral infections and identify CD8 T cell responses and d
124 ld enhance our understanding of hepatotropic viral infections and lead to improved vaccines and thera
125 nctions between symptomatic and asymptomatic viral infections and may partly explain the propensity f
126 lantation monitoring of common opportunistic viral infections and of graft rejection, and should faci
128 response can increase individuals' risk for viral infections and several inflammation-related diseas
129 learned from birth cohort studies examining viral infections and subsequent asthma and from understa
131 in Nfkbia(NES/NES) mice poorly expand during viral infection, and this can be overcome by exogenous I
132 of environmental exposure on the severity of viral infections, and how the viral genome influences ho
133 IFI44L are upregulated after a wide range of viral infections, and IFI44L can serve as a diagnostic b
134 he context of the CNS development, acute CNS viral infections, and post-infectious and noninfectious
135 ns of the two pathways to the attenuation of viral infection are different in mouse versus human cell
136 of intestinal homeostasis.IMPORTANCE Enteric viral infections are a major cause of gastroenteritis wo
142 , additional environmental triggers, such as viral infections, are usually required to initiate the o
143 or health laboratories that seek to identify viral infections as early as possible, optimally at the
146 ar distinctions drawn between enhancement of viral infection at the plasma membrane and amphipathicit
149 provide a possible mechanistic link between viral infection, bloom termination, and mass carbon expo
150 cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, p
151 Both ARVs and NAbs prevent new rounds of viral infection, but NAbs may have the additional capaci
152 ctive in the intestinal epithelium following viral infection, but our understanding of the benefits o
153 to provide quantitative descriptions of many viral infections, but for the Ebola virus, which require
154 ease is strongly associated with respiratory viral infections, but the impact of viruses on Streptoco
155 erge in the development of human cancers and viral infections, but their relevance to bacterial disea
156 region (MPER) results in robust blocking of viral infection by a class of broadly neutralizing antib
157 late innate and adaptive immune responses to viral infection by engaging with receptors on immune cel
159 sting T-cells, SAMHD1 blocks HIV-1 and other viral infections by depletion of the dNTP pool to a leve
160 st innate immunity against hepatitis B and C viral infections by inducing m(6)A modification of viral
162 tal roles in immune defenses against enteric viral infections by integrating diverse signals, includi
163 cate that sphingosine prevents at least some viral infections by interfering with the interaction of
164 lls that facilitate clearance of the initial viral infection can affect host susceptibility to coinfe
170 nfavorable conditions (e.g. tumor hypoxia or viral infection), canonical, cap-dependent mRNA translat
174 in humans and is prototypic of a persistent viral infection characterized by periods of latency.
175 to bumble bees, but evidence of a sustained viral infection characterized by virus replication and a
176 luenza-like illness and laboratory-confirmed viral infection; clinical respiratory illness had incons
177 s integral for mechanistic insights into the viral infection cycle, very little is known about the lo
179 rpesviral protein kinase homologs.IMPORTANCE Viral infection dramatically changes the levels of many
181 n, or uncontrolled inflammation triggered by viral infections during pregnancy, and its potential dow
182 Review highlights the need for understanding viral infection dynamics in realistic physiological and
184 t of granule-mediated cytotoxicity, specific viral infections, excess IL-18, and chimeric antigen rec
186 biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by
187 immunotherapeutic approaches for persistent viral infections.FUNDINGDeutsche Forschungsgemeinschaft
192 We performed serological profiling of the viral infection history in 899 individuals from an NCI-U
194 CE CD8 TCR repertoires responding to chronic viral infections (HIV, hepatitis C virus [HCV], Epstein-
195 (ART) in relation to those of other chronic viral infections (i.e., cytomegalovirus [CMV] and Epstei
196 nds for the potential treatment of influenza viral infections.IMPORTANCE Influenza viruses are highly
197 sional (3-D) human airway tissues to examine viral infection in a physiologically relevant model syst
199 However, the effect of these mutations on viral infection in cell culture and in vivo is not well
200 mary receptor for pathogenic NWAs, enhancing viral infection in guinea pigs.IMPORTANCE JUNV is one of
203 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs.
205 eletion increases cellular susceptibility to viral infection in vitro, and that Snx5 knockout in mice
206 el antivirals for the treatment of influenza viral infections in humans, a search that could be exped
209 NGS to assess the frequencies of alternative viral infections in SARS-CoV-2 RT-PCR-negative PUIs (n =
211 monstrate the differential effect of primary viral infections in the susceptibility to disease exacer
213 o exert different functions in vivo during a viral infection, in a manner tightly orchestrated in tim
214 ents presenting with symptoms of respiratory viral infection, including influenza-like illness (ILI).
223 knowledge of the progression of the initial viral infection is limited, and no safe or effective vac
228 at other functions pDCs exert in vivo during viral infections is controversial, and more studies are
229 chanism by which the pathogenesis of certain viral infections is enhanced in the presence of sub-neut
230 liorate lung inflammation during respiratory viral infections is possible but that the timing and dur
233 of tissue-specific effects of primary acute viral infections like COVID-19 are essential for underst
234 Here, we have shown that upon DNA and RNA viral infection, macrophages reduced 7-dehydrocholestero
235 pes of RNA sensed by RLRs in the contexts of viral infection, malignancies and autoimmune diseases.
236 and the TLR3 pathways in the attenuation of viral infection may be species specific.IMPORTANCE The m
240 in mediating antiviral protection in various viral infections, necessitating a detailed understanding
242 ylate (cOA) second messengers in response to viral infection of bacteria and archaea, potentiating an
245 dentify host factors required for SARS-CoV-2 viral infection of human alveolar epithelial cells.
247 or human LDLRAD3 results in markedly reduced viral infection of neuronal cells, which is restored upo
249 Our findings provide evidence against direct viral infection of the kidneys as the major pathomechani
251 al changes were observed and no evidence for viral infection or integration could be provided after l
253 .51; 95% CI = 4.37-12.91), respiratory tract viral infection (OR = 7.75; 95% CI = 1.60-37.57), cytome
254 ions, either directly, through modulation of viral infection, or indirectly, through alteration of in
256 lar origin, such as bacterial peptidoglycan, viral infections, parasitic infections, activated Rho GT
257 genetic regulation in immune cells following viral infection plays a role in the inflammatory respons
259 tion with implications for understanding how viral infections promote pain and can lead to neuropathi
261 roles of these induced genes in controlling viral infections remain largely unknown, limiting our ab
262 vasion mechanisms, possible drugs to prevent viral infection/replication, and health cares to minimiz
265 universal face masking policy on respiratory viral infections (RVIs) among admitted very-low-birthwei
266 ORTANCE Double-stranded RNAs produced during viral infections serve as pathogen-associated molecular
267 fibrils, known as semen-derived enhancer of viral infection (SEVI), that enhance the viral infectivi
268 pulations provide averaged information about viral infections, single-cell analyses offer individual
271 fully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disea
272 ultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for
273 g prolonged exposure to Ags, such as chronic viral infections, sustained TCR signaling can result in
274 functional insights into the role of ACE2 in viral infection that can potentially be exploited for th
275 attempts to reverse and eliminate the latent viral infection that prevents eradication of the virus.
276 ecent discoveries have revealed that, during viral infection, the presence of the RNA modification N(
277 the relationships between host genetics and viral infections, the contributions of respiratory viral
280 ecificity in distinguishing abnormalities in viral infections, the high sensitivity of CT makes this
281 ugh recombinant EC1 is a potent inhibitor of viral infection, there is no molecular description of th
282 prior or concurrent upper respiratory tract viral infection, this bacterium commonly causes multiple
284 ination was improved by preventing secondary viral infections through a mechanism involving significa
285 infections, the contributions of respiratory viral infections to patterns of immune development, the
287 in response to type I interferons.IMPORTANCE Viral infection triggers the secretion of type I interfe
289 degradation and interferon suppression, and viral infection under interferon-competent conditions.
292 are not enriched for canonical regulators of viral infection, we find that many of these genes do imp
293 d immunity after coronavirus and other acute viral infections, we posit that, with few exceptions, th
294 n of certain biomarkers associated with this viral infection which can be done by simply re-purposing
295 ntial pathogen recognition receptors sensing viral infections while LGP2 has been described as both R
297 gene expression relevant for the control of viral infection, with both proteins potentially facilita
298 ing antibody response is typical of an acute viral infection, with declining neutralizing antibody ti
300 entral nervous system (CNS) is vulnerable to viral infection, yet few host factors in the CNS are kno