Eighty-nine per cent of the participants were originally from the EC, which lies geographically between the WC and KwaZulu-Natal (KZN) provinces. In 2004, the antenatal HIV sero-prevalence for these three provinces was estimated to be: WC 15.4%, EC 28.0% and KZN 40.7% . Infection by HIV, Ascaris and other helminths is widespread in all these provinces, especially under conditions of poverty in under-serviced communities [12–16]. In KZN, more species of helminths are endemic, especially in densely populated areas on the coastal plain .
To ensure logical development of the next phase of our research on possible immunological interaction between helminthiasis and HIV/AIDS, it is necessary to recognise that worm egg excretion status is a secondary variable that cannot be the main basis for analysis. Preliminary local data support this point with regard to Ascaris (which accounted for between 69% and 89% of recalls), as does a lot of published information. In the urban environment, the sero-prevalence of ascariasis can exceed egg-prevalence in children and adults. In a group of 41 women from the same community as the study groups, 51.2% were seropositive in terms of elevated Ascaris-specific IgE, but only 26.3% had eggs in faeces, based on several faecal samples from each adult [unpublished data]. In these adults, there was no association between seropositive status for Ascaris and the presence or absence of eggs in faeces. In 600 children in the same community, Ascaris sero-prevalence was not determined but egg-prevalence was 75% . In a nearby community with better sanitation and housing, 48% of 359 children were seropositive for Ascaris but only 15% were egg-positive, based on two faecal samples per child . Children who were egg-positive were more likely to be Ascaris-seropositive. In these examples from the urban CT environment, an immune response to Ascaris was between two- and three-fold more frequent in both adults and children than the presence of eggs in faeces. In rural areas where complications such as intestinal and duct obstructions by Ascaris are well-known but egg-prevalence studies have not been carried out, the position is likely to be similar.
The results make it clear that before and after sexual transmission of HIV is possible, immune responses to Ascaris antigens (as partly reflected by seropositivity), as well as to other endemic helminths, are likely to be detectable in a large proportion of the population studied. The presence or absence of Ascaris eggs in faeces is of little interpretational value because infection success or failure is determined by immune responses to the antigenic challenge, individual traits and other factors. Components of variation include the frequency of ingestion of embryonated eggs, personal hygiene, habitual behaviour (including geophagia ), anti-Ascaris immune competency or incompetency as determined genetically [34–37], and anergy [1, 2, 6–8]. Therefore, egg excretion is secondary to genetic, environmental and other variables, especially in adults. We contend that to evaluate potential relationships between infection by Ascaris (as well as other soil-transmitted helminths) and HIV/AIDS, research should focus on variables that reflect anti-Ascaris immune responses directly (such as cytokines [6–8, 22, 23, 29–33] and immunoglobulins [6, 8, 26–28]) rather than on the presence or absence of worm eggs in excreta. When anthelmintic treatment is evaluated experimentally in terms of possible effects in relation to co-endemic disease, it is important that egg-negative people be included in deworming because they may be harbouring larval-stage or male Ascaris worms only (that cannot produce eggs), and/or the drug per se may have direct effects on the immune system . In terms of recommendations by the World Health Assembly and the World Health Organisation, this procedure would be ethical and safe [15, 44–47], which supports the idea of a "rapid-impact" package for simultaneously treating several neglected tropical diseases in Africa [48, 49].
Recently-published research results are compatible with our rationale [27–33]. It has been shown that individuals who were persistently susceptible to infection by Ascaris, as demonstrated by excretion of eggs in faeces, were characterised by a weak type 2 immune response profile . After age 11, a strong type 2 profile was associated with increased resistance to infection by Ascaris . A Th2 cytokine (IL-5 or the Eosinophil Differentiation Factor) that initiates a process culminating in eosinophils attacking Ascaris larvae, was significantly elevated in both egg-positive and egg-negative residents where challenge from Ascaris antigens is inevitable due to hyperendemicity; compared to IL-5 levels in people living where Ascaris challenge is unusual . We therefore theorise that the risk of HIV infection could be greater in egg-negative adults (than in egg-positives) if a strong type 2 response  down-regulates anti-viral immune factors under conditions of sustained exposure to Ascaris antigens and other pathogens in Africa [1, 2]. In the same situation, progression to AIDS might sometimes be faster ; and the effectiveness of immunisation against HIV and other diseases may be impaired [1–5, 23–25], especially when the sero-prevalence of ascariasis (and/or other helminthic infections) is high.
In South Africa, co-infection between Ascaris (and/or other helminths) and HIV/AIDS (and/or other non-helminthic diseases) is widespread [13–19, 38, 39, 42, 43]. There may be behavioural and/or sociological reasons for the apparent association between HIV-positivity and recall of intestinal helminthiasis reflected in our results, but these possibilities require further investigation. Since endemic helminthiasis will normally influence the immune environment long before heterosexual transmission of HIV (which is mainly driving the epidemic [1, 17–19]) is possible, all aspects of potential disease interaction need to be researched under local circumstances in prepubertal children and in adults, but comparisons between people who have or do not have helminth eggs in their faeces must not be the primary basis for analysis. Human genetic susceptibility and resistance to ascariasis also need to be taken into consideration [34–37] because inevitable confounding of research results is often ignored.