RAPID PROGRESSION TO INVASIVE CERVIX CANCER IN A WOMAN INFECTED WITH THE HUMAN IMMUNODEFICIENCY VIRUS

1998 ◽  
Vol 91 (Supplement) ◽  
pp. 848-850
Author(s):  
Kevin Holcomb ◽  
Mitchell Maiman ◽  
Therese Dimaio ◽  
Jason Gates
1998 ◽  
Vol 72 (2) ◽  
pp. 1600-1605 ◽  
Author(s):  
Krista K. Steger ◽  
Marta Dykhuizen ◽  
Jacque L. Mitchen ◽  
Paul W. Hinds ◽  
Brenda L. Preuninger ◽  
...  

ABSTRACT Simian-human immunodeficiency virus 89.6PD (SHIV89.6PD) was pathogenic after intrarectal inoculation of rhesus macaques. Infection was achieved with a minimum of 2,500 tissue culture infectious doses of cell-free virus stock, and there was no evidence for transient viremia in animals receiving subinfectious doses by the intrarectal route. Some animals experienced rapid progression of disease characterized by loss of greater than 90% of circulating CD4+ T cells, sustained decreases in CD20+ B cells, failure to elicit virus-binding antibodies in plasma, and high levels of antigenemia. Slower-progressing animals had moderate but varying losses of CD4+ T cells; showed increases in circulating CD20+ B cells; mounted vigorous responses to antibodies in plasma, including neutralizing antibodies; and had low or undetectable levels of antigenemia. Rapid progression led to death within 30 weeks after intrarectal inoculation. Plasma antigenemia at 2 weeks after inoculation (P ≤ 0.002), B- and T-cell losses (P ≤ 0.013), and failure to seroconvert (P ≤ 0.005) were correlated statistically with rapid progression. Correlations were evident by 2 to 4 weeks after intrarectal SHIV inoculation, indicating that early events in the host-pathogen interaction determined the clinical outcome.


2007 ◽  
Vol 81 (23) ◽  
pp. 12775-12784 ◽  
Author(s):  
Christina F. Thobakgale ◽  
Dhanwanthie Ramduth ◽  
Sharon Reddy ◽  
Nompumelelo Mkhwanazi ◽  
Chantal de Pierres ◽  
...  

ABSTRACT Human immunodeficiency virus (HIV)-infected infants in sub-Saharan Africa typically progress to AIDS or death by 2 years of life in the absence of antiretroviral therapy. This rapid progression to HIV disease has been related to immaturity of the adaptive immune response in infants. We screened 740 infants born to HIV-infected mothers and tracked development and specificity of HIV-specific CD8+ T-cell responses in 63 HIV-infected infants identified using gamma interferon enzyme-linked immunospot assays and intracellular cytokine staining. Forty-four in utero-infected and 19 intrapartum-infected infants were compared to 45 chronically infected children >2 years of age. Seventy percent (14 of 20) in utero-infected infants tested within the first week of life demonstrated HIV-specific CD8+ T-cell responses. Gag, Pol, and Nef were the principally targeted regions in chronic pediatric infection. However, Env dominated the overall response in one-third (12/36) of the acutely infected infants, compared to only 2/45 (4%) of chronically infected children (P = 0.00083). Gag-specific CD4+ T-cell responses were minimal to undetectable in the first 6 months of pediatric infection. These data indicate that failure to control HIV replication in in utero-infected infants is not due to an inability to induce responses but instead suggest secondary failure of adaptive immunity in containing this infection. Moreover, the detection of virus-specific CD8+ T-cell responses in the first days of life in most in utero-infected infants is encouraging for HIV vaccine interventions in infants.


1995 ◽  
Vol 171 (3) ◽  
pp. 686-689 ◽  
Author(s):  
O. A. Anzala ◽  
N. J. D. Nagelkerke ◽  
J. J. Bwayo ◽  
D. Holton ◽  
S. Moses ◽  
...  

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