Is it necessary to stop HIV infected mothers breastfeeding? We need a clear-cut decision.

I refer to the timely article by Doherty et al. published in the February issue of the Bulletin of World health Organization (1). It has been seen in Southern India that out of 134 HIV-infected mothers, 81% are a potential source of vertical transmission of HIV and this devastating impact on families is alarming (2). We have no further information on this group of HIV-positive mothers, in particular how many infected mothers are giving birth the HIV-positive babies, and also what is the possibility of HIV transmission by breastfeeding in this group. We need a decision regarding the safety of children breastfeeding from a HIV positive mothers. Should those mothers stop feeding their babies to prevent transmission of HIV? Recent studies revealed that HIV type 1 (HIV-1) in breast milk may not necessarily infect a child through breastfeeding. Again, from a review of several recent publications, it has been reported that there is a possible risk to transmit HIV-1 by breastfeeding, but that the risk is not highly significant. The risk is there, of course, but may be cured with timely anti retroviral therapy treatment of the HIV-positive pregnant mother. The fact is that breastfeeding saves many children, mainly in resource-poor countries where the majority of people cannot afford formula milk or a good substitute to mother’s milk. Eventually, breastfeeding not only protects babies by increasing their immunity to infection, breast milk also prevents under-nutrition and starvation. Breastfeeding is still recommended where infectious diseases are a common cause of childhood death, despite the additional risk of HIV transmission. Unfortunately, there is an ambiguous recommendation “In countries where safe alternatives to breast milk exist, HIV-1 positive mothers should not breast feed their infants. On the other hand, in countries where infectious diseases cause considerable infant death, HIV-1 positive mothers should consider breastfeeding.” (3). We need a clear evidence-based opinion on HIV infected breastfeeding: is it safe or not? Chitta Ranjan Choudhury. REFERENCES: Tanya Doherty et al. Effect of the HIV epidemic on infant feeding in South Africa: "When they see me coming with the tins they laugh at me". Bull World Health Organ 2006;84:90-97 Mayer K et al. Marriage, monogamy and HIV: a profile of HIV-infected women in south India International Journal of STD & AIDS, Volume 11, Number 4, 1 April 2000, pp. 250-253(4) Dunn DT, Newell ML, Ades AE, Peckham CS. Risk of human immunodeficiency virus type 1 transmission through breastfeeding. Lancet: 1992 Sep 5;340(8819):585-8. Epidemiology and Biostatistics Unit, Institute of Child Health, London, UK. Professor Chitta Ranjan Choudhury, Coordinator, International Programme for Tropical Oral Health, Poole Hospital NHS and IHCS, Bournemouth University, Longfleet road, Poole, Dorset BH15 JB, England, UK; and Head, Department of Oral Biology, Centre for Oral Disease Prevention & Control, AB Shetty Memorial institute of Dental Sciences, Deralakatte, Mangalore, India (Email: [email protected])

Antibody and Cytokine Responses in Helicobacter pylori-Infected Various Mouse Strains

Helicobacter pylori (H. pylori) infection in the stomach is etiologically closely associated with chronic active gastritis, peptic ulcer, gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma. In this study, we examined the antibody responses and cytokine profiles of three strains of mice (BALB/c, C3H/He, and C57BL/6) infected with H. pylori. Following this, correlations between host-immune reactions and intensity of inflammation were analyzed. H. pylori (ATCC43504) was intragastrically administered once a week to the mice from 4 weeks of age, and they were sacrificed at the ages of 4 and 7 months. In these mice, we examined the histology of the stomach, antibody titers against H. pylori, and serum levels of cytokines (IL-4, IL-10, TNF-alpha, IL-2 and Interferon-gamma). In BALB/c mice, inflammation of the stomach was minimal. Inflammation was observed in 63.6% of C57BL/6 mice and 33.3% of C3h/He mice. In C57BL/6 and C3H/He mice, all the cytokines tended to increase. In contrast, BALB/c mice were inactive in cytokine production except for IL-2. Two C3H/He mice developed severe inflammation with lymph follicles; one showed a response largely typical of Th-1, and the other showed a response largely typical of Th-2. Although a definite correlation was not shown between Th-1/Th-2 response evaluated by cytokine production and intensity of inflammation, it appears that in H. pylori-induced inflammation both cell-mediated (Th-1) and humoral (Th-2) immunity play a role in pathogenesis.</p