PubMed · 11737366
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M Youle. 2000. Optimizing indinavir regimens.. https://doi.org/10.1046/j.1468-1293.2000.00005.x
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In Yaounde, Cameroon, HIV-1 group-specific V3 serology on 1469 HIV-positive samples collected between 1996 and 2001 revealed that group O infections remained constant around 1% for 6 years. Only one group N sample was identified and 4.3% reacted with group M and O peptides. Although the sensitivity of the group-specific polymerase chain reaction (PCR) in two genomic regions was not optimal, we confirmed, in at least 6 of 49 (12.2%) dual O/M seropositive samples and in 1 of 9 group O samples, dual infection with group O and M viruses (n = 4) or with group O or M virus and an intergroup recombinant virus (n = 3). Partial env (V3-V5) sequences on a subset of 295 samples showed that at least eight subtypes and five circulating recombinant forms (CRFs) of HIV-1 group M co-circulate; more than 60% were CRF02_AG and 11% had discordant subtype/CRF designations between env and gag. Similarly as for subtype B, the proportion of syncytium-inducing strains increased when CD4 counts were low in CRF02_AG-infected patients. The V3-loop charge was significantly lower for non-syncytium-inducing strains than for syncytium-inducing strains but cannot be used as an individual marker to predict phenotype. The two predominant HIV-1 variants in Africa, CRF02_AG and subtype C, thus have different biological characteristics.
OBJECTIVE: To examine the effect of 2 weeks of treatment with prednisone on the incidence of nevirapine-associated rash in HIV-1-infected patients receiving combination antiretroviral therapy. METHODS: This was a 24-week, prospective, randomized, open-label, international study. Patients were randomized to receive nevirapine plus open-label prednisone (40 mg once daily for 14 days) (n = 69) or nevirapine alone (n = 69). All patients received at least two other antiretroviral drugs. Nevirapine was administered at the lead-in dosage of 200 mg once daily. After the initial 2 weeks of the study, the nevirapine dosage was increased to 200 mg twice daily. RESULTS: During the first 6 weeks of treatment, rash was not reduced in the patients who received prednisone: prednisone treatment group, 23 (33%)/69; nonprednisone treatment group, 13 (19%)/69 (one-tailed Fisher exact test for prednisone reducing the incidence of rash, p =.984). There tended to be more severe rashes (7% versus 1%, respectively) and more therapy discontinuations due to rash (16% versus 9%, respectively) in the prednisone treatment group than in the nonprednisone treatment group. Risk factors for rash included higher pretreatment CD4 cell count, lower HIV-1 RNA level, female sex, and higher trough nevirapine concentrations. The prednisone treatment group had a marked increase in the median CD4 cell count in the first 2 weeks, which stabilized at a level similar to that in the nonprednisone treatment group. HIV-1 RNA responses were similar between the two groups. Treatment-naive patients had similar decreases in plasma HIV-1 RNA levels at week 24: approximately 2.3 log(10) copies/mL. CONCLUSIONS: This study demonstrated that 2 weeks of concomitant therapy with prednisone does not decrease the occurrence of nevirapine-associated rash. The use of prednisone is not recommended to prevent rash in patients receiving nevirapine. Prednisone administration had no adverse effects on the virological responses or on CD4 cell count changes at 24 weeks.
The purpose of this study is to clarify the roles of immune cell types, both individually and synergistically, in esophageal squamous cell carcinoma (ESCC). One hundred and twenty-two patients (105 males and 17 females; mean age, 62.3 years) with primary ESCC underwent surgical tumor resection at the Department of Surgical Oncology, School of Medicine, Hokkaido University and two affiliated hospitals between 1989 and 1999. Immunohistochemical analyses were performed for CD4, CD8, and CD57 (surface markers for natural killer cells). Patient prognosis was found to correlate with the number of CD4(+) and CD8(+) T cells in the stroma and the number of CD8(+) T cells within the cancer cell nest. Furthermore, the number of CD8(+) T cells in the stroma and within the cancer cell nest was found to be correlated [correlation coefficient (r) = 0.790; P < 0.0001). However, no correlation was observed between the number of natural killer cells and patient prognosis. Patients were classified into the following four groups based on CD4(+) and CD8(+) T-cell count: CD4/8(+/+), CD4/8(+/-), CD4/8(-/+), CD4/8(-/-). For the general patient pool, as well as for selected p-stage III and IV cases (n = 48), the survival rate for CD4/8(+/+) patients was significantly higher than that for the other three groups (log-rank test, P = 0.0012 and 0.0088, respectively). Multivariate analysis identified CD4/8(+/+) status, T classification, and N classification as independent prognostic factors. In conclusion, cooperation between CD4(+) and CD8(+) T cells correlates strongly with ESCC patient prognosis.