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1                            Here we show that streptococcal 4-aminobenzoate/para-amino benzoic acid (p
2 . pyogenes virulence factor, which we termed streptococcal 5'-nucleotidase A (S5nA).
3 donii and in Escherichia coli expressing the streptococcal accessory Sec system.
4 standing of the predominant features of oral streptococcal adaptive immune repertoires.
5 he beta-sandwich domain seen in the parental streptococcal adhesin, but flanking sequences at both N-
6 otein Epf from S. pyogenes serotype M49 is a streptococcal adhesin.
7 sin, Fap1, demonstrating that BapA1 is a new streptococcal adhesin.
8 cosylation of a family of serine-rich repeat streptococcal adhesins.
9  a mutant deficient in the production of the streptococcal ADP-ribosyltransferase SpyA generates lesi
10                                   Although a streptococcal aldolase, LacD.1, has been adapted to viru
11                                     Although streptococcal and Bacillus UGLs were active on unsaturat
12             In comparison with structures of streptococcal and Bacillus UGLs, a pocket-like structure
13 SC-derived mAb 24.3.1 was found to recognize streptococcal and brain Ags.
14 biotic used as the last resort treatment for streptococcal and staphylococcal bacteria including meth
15 lecular-weight serine-rich proteins found in streptococcal and staphylococcal species and possesses t
16 soriasis activity has been linked to group A streptococcal and viral infections.
17            Affinity purification of the anti-streptococcal antibodies present within pooled immunoglo
18                                          The streptococcal antigen I/II (AgI/II)-family polypeptides
19 ion of the minor fimbrial antigen (Mfa) with streptococcal antigen I/II (e.g., SspB) facilitates colo
20 icate that the Mfa1-interacting interface of streptococcal antigen I/II encompasses both the KKVQDLLK
21  interaction involves the association of the streptococcal antigen I/II with the minor fimbrial antig
22 algorithms used a rapid and specific group A streptococcal antigen test to screen throat specimens, f
23 ecent advances have been made in identifying streptococcal antigens that may play a pathogenic role i
24                              In monoculture, streptococcal arginine biosynthesis was inefficient and
25 erful lysin with potential for treating most streptococcal associated infections.
26          IgG from SC and a related subset of streptococcal-associated behavioral disorders called "pe
27                                              Streptococcal attachment to and entry into epithelial ce
28            The theme of molecular mimicry in streptococcal autoimmune sequelae is the recognition of
29  pathogenesis of rheumatic fever and group A streptococcal autoimmune sequelae of the heart valve and
30                AE reports for viridans group streptococcal bacteremia, a targeted toxicity on AAML053
31 he third Ig-binding domain of protein G from streptococcal bacteria (GB3).
32                                              Streptococcal bacteria use peptide signals as a means of
33  colonized much less efficiently in vitro on streptococcal biofilms than on Actinomyces naeslundii bi
34 latelets directly enhances the resistance of streptococcal biofilms to clindamycin.
35 lonization of S. mutans BM71 on the existing streptococcal biofilms.
36 ults of routine throat cultures on selective streptococcal blood agar plates.
37                   We analyzed 58 recent oral streptococcal bloodstream isolates, and we obtained clin
38 wo conserved group A streptococci (GAS) Ags, streptococcal C5a peptidase and immunogenic secreted pro
39           Autoantibodies against the group A streptococcal carbohydrate epitope GlcNAc and cardiac my
40  GAS-induced IL-17A significantly influences streptococcal carriage and alters local inflammatory res
41                  During the chronic phase of streptococcal cell wall-induced arthritis in rats, compo
42 oinflammation associated with an established streptococcal CNS infection when delivered therapeutical
43 utbreak investigation implicated measles and streptococcal co-infections in most deaths, and also cha
44                                          The streptococcal coaggregation regulator (ScaR) of Streptoc
45                                          The streptococcal collagen-like (Scl) proteins are widely pr
46 ce factors deployed by streptococci includes streptococcal collagen-like (Scl) proteins.
47                                              Streptococcal collagen-like protein 1 (Scl-1) is one of
48 urring polymorphism in the gene encoding the streptococcal collagen-like protein A (SclA) in GAS carr
49 , we characterize an interaction between the streptococcal collagen-like protein Scl1.6 of M6-type gr
50 direct interactions between the cell surface streptococcal collagen-like protein-1 (Scl1) and the hum
51                We recently reported that the streptococcal collagen-like protein-1, Scl1, selectively
52 ot affect triple helix stability of the Scl (Streptococcal collagen-like) protein.
53     Prior treatment with estradiol prolonged streptococcal colonization and was associated with reduc
54 asal vaccine are necessary for prevention of streptococcal colonization.
55 S. bovis groups of species, even though many streptococcal competence genes and the competence regula
56  their viruses in humans, we analysed 13 977 streptococcal CRISPR sequences and compared them with 2
57 oexist at the same time, which suggests that streptococcal CRISPR/Cas systems are under constant pres
58 combining J8-DT with an inactive form of the streptococcal CXC protease, S. pyogenes cell envelope pr
59 lic replacement of the chromosomally encoded streptococcal cysteine protease (speB) in the MGAS5005 D
60                                              Streptococcal cysteine protease (SpeB), the major secret
61                        Expression of SpeB, a streptococcal cysteine protease, is critical for this pr
62 staphylococcal cytolysin alpha-toxin and the streptococcal cytolysin streptolysin O enhanced penetrat
63                               Viridans group streptococcal detection using PHIS microbiology data had
64                                          The streptococcal determinant camG encodes a lipoprotein wit
65 accounted for 34 of the 254 cases of group B streptococcal disease (13.4%).
66 ths); however, 74.4% of the cases of group B streptococcal disease (189 of 254) occurred in term infa
67                          Early-onset group B streptococcal disease (EOGBS) occurs in neonates (days 0
68 in which the newborn had early-onset group B streptococcal disease (i.e., disease in infants <7 days
69            The incidence of invasive group B streptococcal disease among infants from birth through 6
70 f 254 births in which the infant had group B streptococcal disease and 7437 births in which the infan
71  There were 14,573 cases of invasive group B streptococcal disease during 1999-2005, including 1348 d
72                               Severe group A streptococcal disease including acute poststreptococcal
73                                      Group B streptococcal disease is one of the most common infectio
74 babies younger than 7 days) invasive group B streptococcal disease is rectovaginal colonisation of th
75 ever, its importance for the pathogenesis of streptococcal disease is unknown.
76 ad a higher incidence of early-onset group B streptococcal disease than did term infants (0.73 vs. 0.
77 The overall incidence of early-onset group B streptococcal disease was 0.32 cases per 1000 live birth
78 rth through 6 days, the incidence of group B streptococcal disease was lower in 2003-2005 relative to
79 al of 61.4% of the term infants with group B streptococcal disease were born to women who had tested
80 I, III, V) could prevent most global group B streptococcal disease.
81  (day 0-6) and late-onset (day 7-89) group B streptococcal disease.
82  induce complete protection against invasive streptococcal disease.
83 ethod facilitating the prevention of group B streptococcal disease.
84 -based system that monitors invasive group B streptococcal disease.
85 vent additional cases of early-onset group B streptococcal disease.
86 ibitors to be used in prevention of invasive streptococcal disease.
87 ing an extracellular DNase virulence factor (streptococcal DNase D2, SdaD2) and subsequently acquired
88                        The incidence of oral streptococcal endocarditis did not increase (unadjusted:
89 e in staphylolytic activity conferred on the streptococcal endopeptidase domain, and surprisingly the
90  heavy-chain glycan on asparagine 297 by the streptococcal enzyme endo-beta-N-acetylglucosaminidase (
91 ronal cell in Sydenham chorea share a common streptococcal epitope GlcNAc and target intracellular bi
92 oantibodies that target the dominant group A streptococcal epitope of the group A carbohydrate, N-ace
93  expression of the CovRS-controlled secreted streptococcal esterase (SsE).
94 A") protects mice from lethal challenge with streptococcal exotoxin A, as well as from lethal GAS bac
95              We named this protease SepM for streptococcal extracellular protease required for mutaci
96 esults of this study reveal a novel secreted streptococcal factor that, in the absence of SpeB, can t
97 vasive disease have been described, specific streptococcal factors and host properties influencing as
98 tify a putative fibronectin binding protein, streptococcal fibronectin binding protein A (SfbA).
99           To explore the level and extent of streptococcal fomite contamination that children might b
100                                      Group A streptococcal (GAS) infection induces the production of
101 AIP) began surveillance for invasive group A streptococcal (GAS) infections in Alaska in 2000 as part
102                      Surveillance of group A streptococcal (GAS) infections was undertaken as a major
103 s (NSAIDs) contribute to more severe group A streptococcal (GAS) infections, yet a beneficial role fo
104 endations regarding the diagnosis of group A streptococcal (GAS) pharyngitis in adults.
105                                      Group A streptococcal (GAS) pharyngitis is a particularly import
106 g or treating adults at low risk for group A streptococcal (GAS) pharyngitis.
107                             Invasive group A streptococcal (GAS) strains often have genetic differenc
108 on of streptokinase (SK), a critical group A streptococcal (GAS) virulence factor, were identified th
109                  Survivors of infant group B streptococcal (GBS) disease are at risk of neurodevelopm
110             Further reduction in the group B streptococcal (GBS) disease burden in neonates in the Un
111 rain to injury; however, the role of group B streptococcal (GBS) disease has not been reviewed.
112 amining the epidemiology of invasive group B streptococcal (GBS) disease have been undertaken.
113  eighth in a series on the burden of group B streptococcal (GBS) disease, aims to estimate the percen
114 axis (IAP) prevents most early-onset group B streptococcal (GBS) disease.
115                                          All streptococcal genomes encode the alternative sigma facto
116 riginally isolated from a case of acute post-streptococcal glomerulonephritis, is unusually competent
117 des, which are mostly glucans synthesized by streptococcal glucosyltransferases (Gtfs), provide bindi
118 cation schemes within members of the "mitis" streptococcal group.
119 esis was essential for coaggregation-induced streptococcal growth.
120 reptococcus gordonii as a model organism for streptococcal H(2)O(2) production, H(2)O(2)-dependent eD
121 to play a role limited to the penetration of streptococcal HA capsules, facilitating bacterial lysoge
122                         As determined by apo Streptococcal haem-associated protein, Hb had the lower
123                              We evaluate the streptococcal hemoprotein receptor (Shr), a conserved st
124 alysis, we identified the FH receptor as the streptococcal histidine triad (SHT) surface protein.
125 -rich glycoprotein (HRG), and the name sHIP (streptococcal histidine-rich glycoprotein-interacting pr
126 hese results, plus the suspected role of the streptococcal homologue in certain diseases such as acut
127 ith robust activity and an extended-spectrum streptococcal host range against most streptococcal spec
128 ts into the role of complex carbohydrates in streptococcal host-pathogen interaction.
129 een mitral valve prolapse and viridans group streptococcal IE in a population-based cohort from Olmst
130 sociated with an increased incidence of oral streptococcal IE.
131                   Thus, tissue deposition of streptococcal IgA-binding M proteins may contribute to t
132 ulin (IVIG) in treatment of invasive group A streptococcal (iGAS) infection, and the need for prophyl
133 rotease distinct from previous characterized streptococcal immunoglobulin degrading proteases of the
134  and is the main neurologic manifestation of streptococcal-induced rheumatic fever.
135 e neuropsychiatric disorders associated with streptococcal infection (PANDAS).
136                                              Streptococcal infection has been linked with the develop
137 tic shock; for 16 (50%) women with a group A streptococcal infection there was <2 h-and for 24 (75%)
138 e neuropsychiatric disorders associated with streptococcal infection)].
139 icularly with confirmed or suspected group A streptococcal infection, should be regarded as an obstet
140                               During group B streptococcal infection, the alpha C protein (ACP) on th
141 ion of bacterial adaptations during systemic streptococcal infection.
142 of CpsY-dependent regulation during systemic streptococcal infection.
143 ppressed transcription of these genes during streptococcal infection.
144 nique susceptibility of the human species to streptococcal infection.
145 lines focus solely on group A beta-hemolytic streptococcal infection.
146 such as rheumatic heart disease and invasive streptococcal infection.
147 ate of varicella-associated invasive group A streptococcal infections (IGASI).
148 ted with increased risks, although less than streptococcal infections for OCD and any mental disorder
149 H binding in vivo (i.e., for pathogenesis of streptococcal infections), we used our recent finding th
150 describe a mechanism that underpins epidemic streptococcal infections, which have affected many milli
151 s M protein (emm), C5a peptidase (scpA), and streptococcal inhibitor of complement (sic) by directly
152 eptide synthetase (NRPS) system carried by a streptococcal integrative conjugative element (ICE), ICE
153 ture design of small molecular inhibitors of streptococcal invasion.
154                  A total of 155 nonduplicate streptococcal isolates (50 group A, 48 group B, 28 group
155                    Fifty-six alpha-hemolytic streptococcal isolates were identified using MALDI Bioty
156 ative Cpl-7 cell wall binding domains of the streptococcal LambdaSa2 endolysin were replaced by staph
157 ructure revealed a strong resemblance to the streptococcal laminin-binding proteins Lbp and Lmb.
158 ionships between plasminogen-binding group A streptococcal M (PAM) protein and SK2b have been reveale
159 en (Pg)/plasmin receptor, Pg-binding group A streptococcal M protein (PAM), and the human Pg activato
160 d the presence of T cells crossreactive with streptococcal M protein and cardiac myosin.
161                                          The streptococcal M protein that is used as the substrate fo
162  that respond to peptide sequences common to streptococcal M proteins and skin keratins have been det
163 previously shown that IgA-binding regions of streptococcal M proteins colocalize with IgA in mesangia
164 rldwide, regardless of the infecting group A streptococcal M serotype.
165 due internal peptide (VEK-30) from a group A streptococcal M-like protein, the dynamic properties of
166 plasminogen (human Pg (hPg)) binding Group A streptococcal M-protein (PAM) as its major cell surface
167 cal properties of the complex formed between streptococcal M1 and human fibrinogen.
168 e structure and biosynthesis of streptide, a streptococcal macrocyclic peptide.
169 ortant mechanistic implications for the anti-streptococcal macrophage response and sepsis pathogenesi
170 ed membrane protein which is anchored to the streptococcal membrane by an N-terminal transmembrane se
171 with peptide affinity tags is located in the streptococcal membrane.
172 with BBB endothelium and the pathogenesis of streptococcal meningitis.
173 lood-brain barrier and in the development of streptococcal meningitis.
174 ioning to favour carbon sources generated by streptococcal metabolism.
175 hanism of resistance involves sensing of the streptococcal metabolite hydrogen peroxide by A. actinom
176 for IL-17A in contributing to the control of streptococcal mucosal colonization and provide new insig
177 mparable to those for the well-characterized streptococcal natural transformation systems.
178  coli strains through induction of different Streptococcal (p)ppGpp synthetase fragments.
179 ntified a limited level of homology to other streptococcal PAs, including streptokinase; however, Pad
180 eals the potential of PCR/ESI-MS to detect a streptococcal pathogen not captured by conventional cult
181  tools for the understanding of Scl-mediated streptococcal pathogenesis and important structural insi
182    Recently, however, genome-wide screens of streptococcal pathogenesis have identified genes encodin
183         We conclude that SpyA contributes to streptococcal pathogenesis in the mouse subcutaneous inf
184  prompt a reevaluation of the role of SPN in streptococcal pathogenesis.
185                                              Streptococcal pathogens have evolved to express exoglyco
186                                         Many streptococcal pathogens require a polysaccharide capsule
187 own as pili, have been recently described in streptococcal pathogens, including GBS.
188                                              Streptococcal pathogens, such as the group B streptococc
189 gous to CiaR/CiaH, which is present in other streptococcal pathogens.
190 d in stools was highly suggestive of group A streptococcal perianal infection (probability 83.3%).
191 patients with symptoms suggestive of group A streptococcal pharyngitis (for example, persistent fever
192  uncommon at baseline and changed little for streptococcal pharyngitis (intervention, from 4.4% to 3.
193  acute enteritis, 9; Helicobacter pylori, 1; Streptococcal pharyngitis 1; and posttransplant lymphoma
194                                              Streptococcal pharyngitis is still a major infectious di
195 or adult and pediatric patients with group A streptococcal pharyngitis.
196 with antibiotics only if they have confirmed streptococcal pharyngitis.
197 um-positive pharyngitis clinically resembles streptococcal pharyngitis.
198 19179 with acute otitis media; 6746, group A streptococcal pharyngitis; and 4234, acute sinusitis), 4
199  (1100 with acute otitis media; 705, group A streptococcal pharyngitis; and 667, acute sinusitis), 86
200                                The type PI-1 streptococcal pilus is a complex, well studied structure
201 ment of Cpa to target receptors and thus the streptococcal pilus to host cells.
202 is is the largest series to our knowledge of streptococcal PJI managed by DAIR, showing a worse progn
203                      Eligible patients had a streptococcal PJI that was managed with DAIR.
204                         Nephritis-associated streptococcal plasmin receptor and streptococcal pyrogen
205                     The characteristics of a streptococcal plasminogen activator (PA) displaying spec
206 characterised a parallel epidemic of primary streptococcal pneumonia in soldiers without measles.
207 cial for the prevention of diseases, such as streptococcal pneumonia, that are devastating in older p
208 nthesized by conjugation of type III group B streptococcal polysaccharide (GBSIII) to ovalbumin (OVA)
209 le to locus diversification or to changes in streptococcal population structure, yet the composition
210  more frequently than group A beta-hemolytic streptococcal-positive pharyngitis in a student populati
211 ings on the immunoglobulin-binding domain of streptococcal protein G (GB1), these experimental result
212 turally very similar proteins, including the streptococcal protein G and the peptostreptococcal prote
213 ed using the albumin-binding domain (ABD) of streptococcal protein G as a stable protein scaffold.
214 t of the immunoglobulin binding domain B1 of streptococcal protein G, which in its native conformatio
215 ccal hemoprotein receptor (Shr), a conserved streptococcal protein, as a vaccine candidate against GA
216 ected transcript levels of the gene encoding streptococcal proteinase B, a major RopB-regulated virul
217                                        These streptococcal proteins form a structurally distinct subc
218 which we previously demonstrated between the streptococcal proteins Shp and HtsA, may apply in genera
219 ng mechanism of BBK32 and previously studied streptococcal proteins suggests that the binding and ass
220  that CP outcompetes staphylococcal MntC and streptococcal PsaA for Mn(II).
221 a proteinaceous type II TA cassette from the streptococcal pSM19035 plasmid is a member of the epsilo
222 mmunization against the Vbeta8-targeting SAg streptococcal pyrogenic exotoxin A (SpeA), or active imm
223 mages the mucosa to allow for penetration of streptococcal pyrogenic exotoxin A and possibly viable s
224  the phage encoding the SpeA1 variant of the streptococcal pyrogenic exotoxin A superantigen.
225 etration of toxic shock syndrome toxin-1 and streptococcal pyrogenic exotoxin A, respectively, across
226        A secreted cysteine protease known as streptococcal pyrogenic exotoxin B (SpeB) is a key virul
227                                              Streptococcal pyrogenic exotoxin B (SpeB) is a protease
228                                              Streptococcal pyrogenic exotoxin B (SpeB) is an extracel
229 on expression of the extracellular protease, streptococcal pyrogenic exotoxin B (SpeB), capsular hyal
230 ssociated streptococcal plasmin receptor and streptococcal pyrogenic exotoxin B are currently conside
231 s encoding streptococcal superantigen (ssa), streptococcal pyrogenic exotoxins (speC, speH, and speI)
232 equently, we determined that pneumolysin and streptococcal pyruvate oxidase-derived H2O2 production w
233     We found a high sensitivity of a group A streptococcal rapid diagnostic testing (98%) but relativ
234 eract with fibulin-1 and that SOF is a major streptococcal receptor for fibulin-1 but not the only re
235            Eleven strep-EURO and seven other streptococcal reference centers received a panel of 20 c
236              We conclude that VP1 is a novel streptococcal regulatory peptide that controls biofilm d
237 analyzed CRISPR sequences with corresponding streptococcal repeats in order to improve our understand
238                                     Although streptococcal SAgs are known virulence factors in scarle
239                     To determine whether the streptococcal secreted esterase (Sse), an antigen that p
240 oid cells, has to be adapted with respect to streptococcal sensing, handling, and response.
241                                         In a streptococcal sepsis model, this constrained cytokine pr
242 e of HLA-II allelic variations in modulating streptococcal sepsis outcomes and suggest the presence o
243 ed a moribund patient who had beta-hemolytic streptococcal sepsis.
244           Human plasma HDL are the target of streptococcal serum opacity factor (SOF), a virulence fa
245 ibbling mechanism that is similar to that of streptococcal serum opacity factor, which also selective
246 ein that may function as a type of conserved streptococcal shape, elongation, division, and sporulati
247  GAS) freshly isolated from individuals with streptococcal sore throat or invasive ("flesh-eating") i
248  the genomes of strains causing pharyngitis (streptococcal "sore throat").
249 nsporter complex in four different sensitive streptococcal species and demonstrated that it can confe
250 ore, we draw parallels with other pathogenic streptococcal species and provide future research perspe
251                                          All streptococcal species contain the master regulator SigX
252 ral genetic transformation; however, not all streptococcal species have been shown to be naturally co
253 uinis is also the most common viridans group streptococcal species implicated in infective endocardit
254 cci occurs when a lectin-like adhesin on one streptococcal species recognizes a receptor polysacchari
255 voir for many potential pathogens, including streptococcal species that cause endocarditis.
256 ectrum streptococcal host range against most streptococcal species, including S. pyogenes, S. agalact
257 ial sex pheromone system in a commensal oral streptococcal species, which may have implications for i
258 in vitro phenotypes of its homologs in other streptococcal species.
259 nents (PlyCA and PlyCB) that is specific for streptococcal species.
260 shing between atypical pneumococci and other streptococcal species.
261 ) were identified in four different pyogenic streptococcal species.
262 oproteins as virulence determinants in other streptococcal species.
263 e the differential expression of arcA in two streptococcal species.
264 ve, the most common being Staphylococcal and Streptococcal species.
265 treptococcus oralis, the choline-independent streptococcal strain that served as the DNA donor in the
266     Genome sequencing of an additional 1,125 streptococcal strains and virulence studies revealed tha
267  caused by multidrug-resistant neisserial or streptococcal strains.
268                                          The streptococcal studies showed much higher MIC/MBC results
269 e oxidative stress-adaptive responses by the streptococcal subfamily of PerR.
270 dherence and subsequent biofilm formation on streptococcal substrates.
271 ND.1 to PhiM23ND.4, harboring genes encoding streptococcal superantigen (ssa), streptococcal pyrogeni
272 ndrome (TSS) is caused by staphylococcal and streptococcal superantigens (SAgs) that provoke a swift
273 eptococcus sepsis by modulating responses to streptococcal superantigens (Strep-SAgs).
274                        Here we show that the streptococcal surface protein SfbI mediates covalent int
275                               In particular, streptococcal surface proteins have been implicated as p
276                             Isolation of the streptococcal surface proteins recognised by pooled huma
277 by virtue of repetitive sequences-designated streptococcal surface repeats.
278                  Individuals with a positive streptococcal test result had an increased risk of any m
279 21 girls and 547922 boys), 638265 received a streptococcal test, 349982 of whom had positive test res
280 < .001), compared with individuals without a streptococcal test.
281 on on individuals with the registration of a streptococcal test.
282 cebo arm due to ineligibility arising from a streptococcal throat infection and one in the lumacaftor
283 DAS hypothesis found that individuals with a streptococcal throat infection had elevated risks of men
284 l disorder and OCD was more elevated after a streptococcal throat infection than after a nonstreptoco
285  specifically OCD and tic disorders, after a streptococcal throat infection.
286 type of psoriasis is usually associated with streptococcal throat infections and mainly occurs in HLA
287  of chronic psoriasis can be associated with streptococcal throat infections, and T cells that respon
288 ith protection from erysipelas (n = 278) and streptococcal tonsillitis (n = 209) compared with contro
289  from patients with flares associated with a streptococcal tonsillitis and with the HLA-Cw6 allele (c
290 can Heart Association regarding treatment of streptococcal tonsillo-pharyngitis were revised.
291                  For antibiotic treatment of streptococcal tonsillopharyngitis the recommendations fo
292                                              Streptococcal toxic shock syndrome (STSS) and necrotizin
293 a patient with necrotizing fasciitis (NF) or streptococcal toxic shock syndrome (STSS).
294 severe invasive disease in humans, including streptococcal toxic shock syndrome and necrotizing fasci
295  Eighty-four cases of severe iGAS infection (streptococcal toxic shock syndrome, necrotizing fasciiti
296 t case of S. suis arthroplasty infection and streptococcal toxic shock-like syndrome due to an nonenc
297 sults have bearing on the pathophysiology of streptococcal toxic shock.
298 ted upon endolysosomal processing of group B streptococcal type III polysaccharide coupled to a carri
299                          Previously reported streptococcal virulence genes, such as mga, hasA, amrA,
300 ign of future studies of M protein function, streptococcal virulence, epidemiological surveillance, a

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