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1 e with 5 x 10(5) focus-forming units of ZIKV intravaginally.
2 esult in viremia in naive females inoculated intravaginally.
3 n sacral ganglia from guinea pigs vaccinated intravaginally.
4 single and repeated doses of MB66 when used intravaginally.
5 eu5Ac9N(3), and CMP-Leg5,7Ac(2) administered intravaginally (10 mug/d) to N. gonorrhoeae-colonized mi
7 fected with HSV-2 intravaginally and treated intravaginally 24 h later with 100 microg DNA encoding I
8 lt3-L) was found to enhance translocation of intravaginally administered DCs to draining lymph nodes
10 tics of virus spread, we inoculated macaques intravaginally and euthanized them after 2, 4, 7, and 15
11 When bacterial burdens were equivalent in intravaginally and transcervically infected mice at late
13 intravenously or mucosally (intranasally or intravaginally) and then challenged intravaginally with
15 as shown promise as antiherpetics, including intravaginally applied CpG-containing oligodeoxynucleoti
18 cells, was detected in all hCD4/R5/cT1 mice intravaginally challenged with an HIV-1 infectious molec
21 eic dendritic cells did not induce responses intravaginally even in ovariectomized mice in the absenc
22 r of the genital tract, rhesus macaques were intravaginally exposed to cell-free simian immunodeficie
23 l, the insertion of pre-cooled magnetic rods intravaginally for short periods over 3 days, reduced th
25 onses were compared in female mice immunized intravaginally (i.vag.) or intranasally (i.n.) with a ba
26 , BALB/c or congenic SCID mice were infected intravaginally (i.vag.) with the HSV type 2 (HSV-2) vhs
27 to either peptide Ag or male cells delivered intravaginally in ovariectomized mice, but this response
28 ls, bacteria were inoculated in mouse either intravaginally in the last trimester of pregnancy or sys
29 itope (gB(498-505)), and both were delivered intravaginally in the progesterone-induced B6 mouse mode
31 amydia-infected mice, and in initial studies intravaginally infected wild-type, IL-10(-/-), IL-4(-/-)
33 rol of a CD4 promoter (JR-CSF/hu-cycT1) were intravaginally infected with HSV-2 and evaluated for dis
38 ) T cells followed by development of AIDS in intravaginally inoculated macaques and thus provides a h
39 tics of retroviral recombination in vivo, we intravaginally inoculated rhesus macaques, either simult
40 e with pathogenic SIV, all five animals were intravaginally inoculated twice with pathogenic SIV-mac2
41 (-/-), IL-17RA(-/-) and IL-22(-/-) mice were intravaginally inoculated with Candida, and vaginal lava
42 was eventually found in four of six animals intravaginally inoculated with the two SIVmac239 deletio
43 1 (HIV-1) env/rev and gag/pol were delivered intravaginally (IVAG) and intramuscularly (IM) to 2 preg
45 us macaques inoculated intravenously (IV) or intravaginally (IVAG) with a genetically heterogeneous S
46 arious mucosal routes-oral, intrarectal, and intravaginally (ivag)-followed by a systemic or mucosal
48 sis of tissues of rhesus macaques inoculated intravaginally or i.v. with SIV supports the proposed ro
50 used to quantify lachrymal secretions, were intravaginally placed in untreated ovary-intact mice, DM
51 HeJ mice were either sham or INP0341 treated intravaginally pre- and postinoculation with 5 x 10(2) i
52 In this study, a therapeutic vaccine given intravaginally resulted in significantly better protecti
53 l mucosa, while the same antibodies injected intravaginally significantly reduced Thy-1+ T cells in b
54 in which female rhesus macaques were exposed intravaginally to a high dose of simian immunodeficiency
56 re significantly greater in macaques exposed intravaginally to lower rather than higher inoculum dose
58 served only in macaques that were challenged intravaginally twice within the same day with a high dos
60 nnate immunity-deficient C3H/HeJ female mice intravaginally with a human serovar D urogenital isolate
62 pre-treated with progesterone and inoculated intravaginally with artificial insemination fluid from Z
64 l 12:12 light: dark (LD) cycle were infected intravaginally with Chlamydia muridarum either at zeitge
66 into syngeneic naive animals and challenged intravaginally with Chlamydia, recipients of IM immuniza
67 mia, nonobese diabetic (NOD) mice inoculated intravaginally with clinical C. glabrata isolates were s
68 protein, delivered either intramuscularly or intravaginally with CpG and alum adjuvants, (i) boosted
69 g from 5 to 14 weeks of age, were inoculated intravaginally with different doses of the Chlamydia tra
70 Chlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2
71 t this hypothesis, we treated rhesus monkeys intravaginally with either the TLR9 agonist, CpG oligode
73 2Rgamma(-/-)) (NSG)-BLT mice were inoculated intravaginally with HIV and were monitored for plasma vi
74 or the licensed HPV vaccines and challenged intravaginally with HPV6, HPV16, HPV26, HPV31, HPV33, HP
75 O 2000 gel protected 100% of mice challenged intravaginally with HSV-2 introduced in PBS, whereas onl
79 rogesterone or estradiol and then inoculated intravaginally with M. genitalium type strain G37 or a c
82 ult female macaques that had been inoculated intravaginally with pathogenic SIVmac251 became transien
83 lowing vaccination, macaques were challenged intravaginally with repeated weekly low doses of SIV(mac
86 ciency virus (SHIV) 89.6 and then challenged intravaginally with SIVmac239 controlled viral replicati
87 Four female rhesus macaques were inoculated intravaginally with SIVmac251, and then killed 2, 5, 7,
88 e TNF-alpha response in guinea pigs infected intravaginally with the guinea pig strain of Chlamydia p
89 feron gamma gene-deficient C57 mice infected intravaginally with the mouse pneumonitis agent of Chlam
91 L/6), treated with progesterone and infected intravaginally with the mouse pneumonitis strain of Chla
92 R2) protein (Prime) and subsequently treated intravaginally with the neurotropic adeno-associated vir
93 model, rhesus macaques (RM) were inoculated intravaginally with two or three HSV-2 strains (186, 333
94 oth B7-1 and B7-2 (B7KO mice), when infected intravaginally with virulent herpes simplex virus type 2
96 reated with 17-beta-estradiol and inoculated intravaginally with wild-type gonococcal strain FA1090 o
97 ceptibility to N. gonorrhoeae and inoculated intravaginally with wild-type gonococci or a catalase (k
99 highly attenuated in wild-type mice infected intravaginally, with reduced mucosal replication, diseas