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1 EE, along with 11 cases of VEE and 1 case of dual infection.
2 ners as independent risk factors for HBV-HCV dual infection.
3 th the initial isolate failed to result in a dual infection.
4 l burdens, manifestations of disease, and/or dual infection.
5 pe B, 4.3% B/CRF01_AE recombinants, and 0.5% dual infections.
6 mpeting viruses in a single infection versus dual infections.
7 dial infection, 3 trichomoniasis), and 4 had dual infections.
8 high-risk sexual behavior was the source of dual infections.
11 /=1:8) was higher in cases of yaws (63%) and dual infections (92%) than in H ducreyi infections (29%;
12 types along with samples from three cases of dual infection (A(2254)+G(2254)) were correctly identifi
13 mary quarters there were naturally occurring dual infections, although this was identified in only 0.
14 terval [CI], 75 to 133) in participants with dual infection and 68 months (95% CI, 60 to 76) in parti
15 strate a window period for susceptibility to dual infection and indicate that protection from retrovi
17 OBAS-positive specimens (82%), including six dual infections, and identified N. gonorrhoeae in 102 (5
19 present in the lymph nodes of patients with dual infection as compared with lymph nodes from HIV(+)
21 f HLA-B*57/B*5801 escape, a highly sensitive dual-infection assay that uses synonymous nucleotide seq
24 association between severe bronchiolitis and dual infection by human metapneumovirus (hMPV) and human
25 were significantly steeper for patients with dual infection compared with patients with single infect
26 gions either from the FRP system or from the dual infection culture, and very few from the HIV epidem
29 Human immunodeficiency virus type 1 (HIV-1) dual infection (DI) has been associated with decreased C
30 el for KSHV infection and find that EBV/KSHV dual infection enhanced KSHV persistence and tumorigenes
31 hanced ability of the Abbott assay to detect dual infections, especially in the presence of large amo
33 ggest a potential novel hypothesis involving dual infections for the adaptation of heterologous rotav
35 l, 20 out of 22 piglets in the PRRSV-S. suis dual-infection group died within 1 week after challenge
40 ession was most evident in participants with dual infection in whom HIV-2 infection preceded HIV-1 in
43 ited by concomitant HIV-2 infection and that dual infection is associated with slower disease progres
44 e complex and that the observable outcome of dual infection is dependent on the target cell type.
45 llagen I in the adjacent interstitium in the dual infection may facilitate dissemination of H. somni
46 ngs, HIV-1 recombinants generated from these dual infections may be used as a model for in vivo inter
48 HBV-HCV viral interactions in patients with dual infection necessitates careful but aggressive clini
49 sitive cohort in Cameroon exhibits a rate of dual infection of 11% per year, signifying that these in
50 uential plasma obtained before and after the dual infection of 4 subjects were compared to those of m
51 biologic analysis revealed the presence of a dual infection of CMV and specific bacterial plaque.
53 follow-up were characterized with regard to dual infection or single infection and to coreceptor use
56 ased at a lower rate among participants with dual infection, reflecting slower disease progression.
57 was significantly lower in participants with dual infections than in those with HIV-1 infection alone
58 gs, we hypothesized that among patients with dual infection the control of HIV-1 is associated with t
63 ions in patients with yaws and in those with dual infection were larger than those in patients infect
70 lous atrophy (jejunum and/or ileum), whereas dual infection with both viruses induced lesions through
72 .8% (95% confidence interval, 4.5%-7.1%) had dual infection with HBV (hepatitis B surface antigen-pos
78 an: the blood-stage population dynamics of a dual infection with Plasmodium malariae and Plasmodium f
82 otoxigenic Escherichia coli, indicating that dual infections with this leading bacterial cause of TD
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