Sickle cell disease or sickle cell anemia is a common genetic disorder, autosomal recessively. The first medical description was made 1904 by James Herrick. It is characterized by an alteration of hemoglobin, abnormal hemoglobin S whose structure was identified in 1949 by Linus PAULING.
In the Democratic Republic of Congo (including in Lubumbashi), the prevalence of sickle cell trait βA/βS varies between 20% to 30%  and that of sickle cell disease βS/βS is 1.4%  .
Sickle cell disease is a major public health problem in the city of Lubumbashi and Kinshasa. In the Democratic Republic of Congo, HIV seroprevalence was 1.1% according to DHS 2013-2014.
Many studies have shown that HIV seroprevalence among sickle cell anemia was low despite multiple blood transfusions they undergo     .
In our previous work, we have demonstrated the existence of two mandatory mutations in homozygous sickle cell Africans mutation βS/βS and mutation Duffy-46C/C). During HIV infection, the impact of the sickle cell mutation is predominant with respect to susceptibility to HIV (low susceptibility), and it is the result of the double mutation with respect to the progression of viral infection: slow progression  .
The aim of our study was to document the susceptibility of HIV in sickle cell anemia Duffy-46C/C in Kinshasa and Lubumbashi.
2. Materials and Methods
The research targeted topics attending care centers sickle cell in the city of Lubumbashi in the general referral hospital Jason Sendwe and in Kinshasa the Joint Medical Center and anemia SS (CMMASS) in Mabanga Yolo South and Polyclinic Saint Crispin in Ngaliema.
The study population consisted of 505 subjects homozygous sickle cell disease including 235 males and 270 females, aged 1 year to 65 years (age moyen 15, 6 years). SS anemia was determined by the Emmel test and confirmed by acid pH hemoglobin electrophoresis on cellulose acetate gel. Inclusion criteria were HIV/ AIDS positive serology and exclusion criteria were the presence of other viral infections and children under 1 year. The statistical population in this study consisted of any sickle cell patient who had presented to the selected health facilities. This study was conducted over a period from November 5, 2015 to September 22, 2016.
The study was to determine the seroprevalence of HIV among sickle cell anemia Duffy-46C/C for anti HIV antibody tests Determine HIV1/2 test Uni-Gold, confirmed by measurement of viral load technology Abbott Real Time HIV1/2 and determination of CD4 + levels. A data collection sheet was established for information on certain variables, including the number of blood transfusion, age, sex, antiretroviral treatment, vaso occlusive crisis (VOC) or not and the mode of transmission HIV. 5 ml of whole blood were collected in EDTA anticoagulant and plasma was obtained after centrifugation of 3000 revolutions/ minute for 10 minutes at room temperature, 25˚C. The plasma was stored at −20˚C for determination of viral load.
Statistical analyzes were performed with the following tests: Fischer exact test or chi-square, frequency and average. The software Epi Info, SPSS, Excel and Windows 7 were used. The statistical significance threshold was calculated and defined at p < 0.05.
The limitations of our study were to find homozygous sickle-cell anemia with a positive HIV serology. The authorization of the ethics committee has given us before conducting this study (No. approval: UNILU/EMC/071/2017.
The results of HIV seroprevalence are shown in Table 1: six cases of 505 samples were found positive 1.19%.
The results of HIV distribution by age group are shown that the positive cases were found in the age group of 1 to 10 years (3 cases), 11 to 21 years (1 case) and that of 22 to 32 years (2 cases). After these ages no positivity was detected (Table 2).
Table 1. HIV Prevalence homozygous sickle cell Duffy-46C/C.
Table 2. Distribution of sickle-cell anemia by age.
The results of this table are shown that the majorities were female, 5 out of 6 cases (Table 3).
The frequency distribution according to age groups shows that SCD 199 were in the age group from 11 to 21 years, 199 (39.41%) of 505 (Table 4).
The results in this table show that 70.39% received between 1 and 5 blood transfusions (Table 5).
The number of blood transfusion between 1 to 5 revealed more positive HIV cases, 4 cases of 6 and 466 sickle cell patients had previously received at least one blood transfusion and 39 others had never had a blood transfusion (Table 6).
The results according to the clinical profile indicate that 271 sickle cell patients were CVO crises, among them two positive cases of HIV and 234 others were without crisis four positive cases of HIV at the time of blood collection (Table 7).
The results of viral load shows detectable 4 cases, 3.14 Log, Log 2.43, 5.38 log, 3.60 Log and 2 cases undetectable. Among the detectable 4 cases, 3 were naive to ARV. And 2 cases were undetectable on ART. The determination of CD4 + levels shows high values over 500 c/.mu.l ranging from 543 to 893 c/μl in all sickle cell anemia HIV + (Table 8).
Table 3. Distribution of sickle-cell anemia by sex.
Table 4. Positive serology according to age groups.
Table 5. Frequency allocation according to the number of slices blood transfusion.
Table 6. Positive serology as number of blood transfusions slices.
Table 7. Distribution of frequencies according to the clinical profile.
Table 8. Results of viral load of sickle cell anemia Duffy-46C/C.
Our study aimed to document the susceptibility of HIV in sickle cell anemia Duffy-46C/C, show that HIV prevalence is low. These results confirm those found by NGALY et al. 1987  , or 5.4% versus > 10% by Lukuni et al. 1989  , or 5.5% vs. > 10%, and Neto et al. 2010  , (or 0.8% compared to other infections (13.4% HCV, HTLV-1 4.7%, HBV 3.1% and 2.8% Chagga disease) and Tshilolo et al. 2010, 2012   , which years larger multicenter trials including countries in Central Africa (DRC, Gabon and Cameroon), the risk of viral infections (HIV, HBV, HCV) in sickle cell anemia βS/βS showed firstly that the prevalence of HIV infection was significantly reduced compared to that of the normal population (16.5% versus 22%) and secondly that they (sickle cell anemia βS / βS) became slow progressors to viral infection. These results corroborate those found by Mehdi et al. 2012  , 1.5% versus 3.3% and maintain that sickle cell anemia is associated with a lower risk of coinfection with HIV, and this protection against HIV infection may be related to defense immune reinforced in SCD against HIV. These results also similar to those found by Stephen et al. 2012  confirming the study Mehdi et al. 2012  on the low HIV seroprevalence among African Americans with sickle cell disease, and attest that the low prevalence could be related to the inhibition of viral replication of HIV, due to the persistence of inflammation, metabolism Fe immunological changes in sickle cell disease. Our results also confirm those found by Diarra et al. 2013  , 1% versus 3% 1% HBV and HCV, a study in Mali on the prevalence of HIV, HBV and HCV in sickle cell before and after blood transfusion. Among the positive sickle HIV, 5 of 6 were women and most of the positive cases (4/6) were in the range of transfusion number from 1 to 5. These results corroborate those found by Ngo Sack  who showed that all positive patients have already been transfused HIV status increased with the number of blood transfusion.
We also determined the rate of CD4 + and our results reveal CD4 + high rates over the 500 c/μl in all sickle cell anemia Duffy βS/βS HIV +. These results confirm those found by Bagasra et al.  who pioneered the study of pathophysiological mechanisms in HIV infection in sickle cell anemia βS/βS. Their works based on viral load during infection have shown that AIDS progresses much more slowly in the βS/βS patients.
In tracking a small cohort, the authors showed that 44% of βS/βS patients (8 of 18) were long-term asymptomatic with a high CD4 count and a low viral load. In the control group, only 13.9% (5 of 36) were asymptomatic long-term, although in our study, we noticed that some homozygous sickle cell patients had a viral load a little high. These sickles were naive to antiretroviral treatment and had a recent viral infection. This study opens the door to other opportunities, for example, conduct a study of the pathophysiological mechanisms of the double mutation in homozygous sickle cell βS/βS Duffy-46C/C in order to understand the low susceptibility to HIV in sickle cell or the protective effects vis-à-vis HIV in sickle cell.
Most HIV positive sickle cell diseases were infected by blood transfusion, with the exception of a single case, contaminated by mother to child transmission.
The blood transfusion remains a risk in the transmission of HIV/AIDS among people polytransfusees, due probably to the window door. We will have to strengthen blood safety by equipping laboratories and blood banks with reliable early tests that detect viral RNA of HIV.
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