Association Between Unplanned Pregnancy and HIV Seropositivity Disclosure to Marital/Cohabitating Partner Among Post-natal Women in Lusaka, Zambia

Background: Disclosure of a positive HIV result to partner is an important step towards prevention of infection, early diagnosis and optimum care especially in the context of PMTCT. Little is known about the disclosure patterns of postnatal women in relation to planning status of index pregnancy. This study explored this aspect.Objectives: To determine any association between unplanned pregnancy and HIV seropositivity disclosure to stable partner among postnatal women in Lusaka.Design: Using a cross-sectional study design the disclosure patterns of 100 postnatal women with unplanned pregnancies were compared to a similar group of 100 women with planned pregnancies.Results: The crude OR for disclosure of a positive HIV result to partner (planned pregnancy/unplanned pregnancy) was 1.839 (CI= 1.002-3.372). After adjusting for participant and partner's feelings after pregnancy discovery, partner's occupation, condom use in the relationship and length of stay with partner this OR was 2.835 (CI=0.690 -11.643). 66.7% of those that reported that their partners had worries, depression or sadness after disclosure had unplanned pregnancies whereas 83.3% of those that expressed no emotions had planned pregnancies.Conclusions: Possibility of antenatal HIV seropositivity disclosure to partner is the same whether the pregnancy is planned or not. Unplanned pregnancy is associated with more negative reactions by partner after disclosure

Securitisation and its application to low cost housing finance in South Africa

Section 26 of the Constitution of South Africa Act 108 of 1996 provides that housing is a basic human right and that the government must take reasonable legislative and other measures to achieve the realisation of this right. A number of measures were taken to try to resolve this socio-economic issue. A number of housing institutions were established , various pieces of legislation were passed and housing subsidies were provided. However, housing backlogs remain a challenge. In March 1994 the housing backlog was estimated between 1,3 and 1,8 million units. When more than a million houses were provided by 2001 , the housing backlog had increased to between 2 and 3 million houses. To date subsidies in excess of R29 billion have been spent on housing provision. A study by the Department of Housing concluded that, at the current rate of increase of housing funding vis-a-vis the growing backlog and rapid urbanisation, the household backlog will not be changed in ten years' time. The United States of America (USA) had a similar low cost housing problem, but securitisation alleviated it with the participation of government agencies Fannie Mae, Ginnie Mae and Freddie Mac. In South Africa, the NHFC tried to emulate the USA model by establishing Gateway Home Loans (Pty) Limited (Gateway) in 1999. Gateway, however, was not a success. This research investigates whether securitisation can be applied in South Africa to alleviate the low cost housing issue. The study finds that there is a credit availability gap for the low income sector earning less than R8 000 per month because of the perceived risk of default and unwillingness by banks to lend to this sector. The increase in housing backlog that continues unabated, inadequate housing finance system to low income earners, the lessons learnt from the failure of Gateway, the success factors of the USA securitisation model and the sound and sophisticated South African financial system are the rationale for applying securitisation. A proposal of how to effectively apply securitisation to low cost housing in South Africa is provided with recommendations to revive the primary market

CTL Escape Mediated by Proteasomal Destruction of an HIV-1 Cryptic Epitope

Cytotoxic CD8+ T cells (CTLs) play a critical role in controlling viral infections. HIV-infected individuals develop CTL responses against epitopes derived from viral proteins, but also against cryptic epitopes encoded by viral alternative reading frames (ARF). We studied here the mechanisms of HIV-1 escape from CTLs targeting one such cryptic epitope, Q9VF, encoded by an HIVgag ARF and presented by HLA-B*07. Using PBMCs of HIV-infected patients, we first cloned and sequenced proviral DNA encoding for Q9VF. We identified several polymorphisms with a minority of proviruses encoding at position 5 an aspartic acid (Q9VF/5D) and a majority encoding an asparagine (Q9VF/5N). We compared the prevalence of each variant in PBMCs of HLA-B*07+ and HLA-B*07- patients. Proviruses encoding Q9VF/5D were significantly less represented in HLA-B*07+ than in HLA-B*07- patients, suggesting that Q9FV/5D encoding viruses might be under selective pressure in HLA-B*07+ individuals. We thus analyzed ex vivo CTL responses directed against Q9VF/5D and Q9VF/5N. Around 16% of HLA-B*07+ patients exhibited CTL responses targeting Q9VF epitopes. The frequency and the magnitude of CTL responses induced with Q9VF/5D or Q9VF/5N peptides were almost equal indicating a possible cross-reactivity of the same CTLs on the two peptides. We then dissected the cellular mechanisms involved in the presentation of Q9VF variants. As expected, cells infected with HIV strains encoding for Q9VF/5D were recognized by Q9VF/5D-specific CTLs. In contrast, Q9VF/5N-encoding strains were neither recognized by Q9VF/5N- nor by Q9VF/5D-specific CTLs. Using in vitro proteasomal digestions and MS/MS analysis, we demonstrate that the 5N variation introduces a strong proteasomal cleavage site within the epitope, leading to a dramatic reduction of Q9VF epitope production. Our results strongly suggest that HIV-1 escapes CTL surveillance by introducing mutations leading to HIV ARF-epitope destruction by proteasomes

The effect of HIV-1 polymorphism on CD8+ T-cell antigen recognition

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Mukadzi unoerei-ko? (What is your surname)

Sorry, sorry, sorry. What is the woman's surname? My surname is this child. The legs are burnt with the porcupine. What kind of 'mungu' is that, another? I have lost, I have burnt my child. Call his aunt. His aunt where is she? She digs in the chief's garden. Lift the deep voice, we pass. We will come out at Chanembe. Chanembe where there are girls. Who stab each other with knives. The spears are buried under ground . Please give us those spears. We will stab the big tree trunk. The big tree trunk, where is it? It is at the pool of Buuro. What did you give to Buuro? We gave him that little drum there. How does it sound? 'Ti-ndi-ngu!' Hippo in the pool. Where is the owner of the pool? He has gone to pick fruit. We will eat it at our home. Etc., etc

Mukadzi unoirei-ko

A recited nonsense verse

An unusual complication of colitis

An 18-year-old man with a 13 month history of ulcerative coltis (UC) was admitted with a progressive history of worsening left-sided abdominal pain, diarrhoea, rectal bleeding and weight loss. UC had been diagnosed on flexible sigmiodoscopy and biopsies, which confirmed moderately active colitis to the point of insertion (distal descending colon). Initially he was commenced on mesalazine and steroids, but his disease remained active and azathioprine was introduced after 4 months. Despite this he continued to suffer active symptoms, and a colonoscopy was performed after 8 months. This demonstrated some improvement, with mildly active colitis evident to the sigmoid. The full extent of his colitis was not established as the procedure was limited to the sigmoid because of patient discomfort. Over the next 4 months his condition and blood tests gradually worsened to the point that he required admission. On examination, he was feverish and tachycardiac. Abdominal palpation demonstrated a left lower quadrant “mass” and tenderness, but no guarding. Laboratory analysis identified a microcytic anaemia (haemoglobin 5.6 g/dl), normal white cell count, elevated platelet count (666×109/l), raised C-reactive protein (199 mg/l) and a low albumin (23 g/dl). An abdominal radiograph showed right-sided faecal loading. He failed to improve, despite treatment with hydrocortisone and intravenously, and a CT scan of his abdomen and pelvis was requested (figure 1)

CD8+ T cell epitope-flanking mutations disrupt proteasomal processing of HIV-1 Nef.

CTL play a critical role in the control of HIV and SIV. However, intrinsic genetic instability enables these immunodeficiency viruses to evade detection by CTL through mutation of targeted antigenic sites. These mutations can impair binding of viral epitopes to the presenting MHC class I molecule or disrupt TCR-mediated recognition. In certain regions of the virus, functional constraints are likely to limit the capacity for variation within epitopes. Mutations elsewhere in the protein, however, might still enable immune escape through effects on Ag processing. In this study, we describe the coincident emergence of three mutations in a highly conserved region of Nef during primary HIV-1 infection. These mutations (R69K, A81G, and H87R) flank the HLA B*35-restricted VY8 epitope and persisted to fixation as the early CTL response to this Ag waned. The variant form of Nef showed a reduced capacity to activate VY8-specific CTL, although protein stability and expression levels were unchanged. This effect was associated with altered processing by the proteasome that caused partial destruction of the VY8 epitope. Our data demonstrate that a variant HIV genotype can significantly impair proteasomal epitope processing and substantiate the concept of immune evasion through diminished Ag generation. These observations also indicate that the scale of viral escape may be significantly underestimated if only intraepitope variation is evaluated