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      Inactivation of HIV-1 in breast milk by treatment with the alkyl sulfate microbicide sodium dodecyl sulfate (SDS)

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          Abstract

          Background

          Reducing transmission of HIV-1 through breast milk is needed to help decrease the burden of pediatric HIV/AIDS in society. We have previously reported that alkyl sulfates (i.e., sodium dodecyl sulfate, SDS) are microbicidal against HIV-1 at low concentrations, are biodegradable, have little/no toxicity and are inexpensive. Therefore, they may be used for treatment of HIV-1 infected breast milk. In this report, human milk was artificially infected by adding to it HIV-1 (cell-free or cell-associated) and treated with ≤1% SDS (≤10 mg/ml). Microbicidal treatment was at 37°C or room temperature for 10 min. SDS removal was performed with a commercially available resin. Infectivity of HIV-1 and HIV-1 load in breast milk were determined after treatment.

          Results

          SDS (≥0.1%) was virucidal against cell-free and cell-associated HIV-1 in breast milk. SDS could be substantially removed from breast milk, without recovery of viral infectivity. Viral load in artificially infected milk was reduced to undetectable levels after treatment with 0.1% SDS. SDS was virucidal against HIV-1 in human milk and could be removed from breast milk if necessary. Milk was not infectious after SDS removal.

          Conclusion

          The proposed treatment concentrations are within reported safe limits for ingestion of SDS by children of 1 g/kg/day. Therefore, use of alkyl sulfate microbicides, such as SDS, to treat HIV1-infected breast milk may be a novel alternative to help prevent/reduce transmission of HIV-1 through breastfeeding.

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          Most cited references48

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            Effect of breastfeeding on infant and child mortality due to infectious diseases in less developed countries: a pooled analysis. WHO Collaborative Study Team on the Role of Breastfeeding on the Prevention of Infant Mortality.

            (2000)
            The debate on breastfeeding in areas of high HIV prevalence has led to the development of simulation models that attempt to assess the risks and benefits associated with breastfeeding. An essential element of these simulations is the extent to which breastfeeding protects against infant and child mortality; however, few studies are available on this topic. We did a pooled analysis of studies that assessed the effect of not breastfeeding on the risk of death due to infectious diseases. Studies were identified through consultations with experts in international health, and from a MEDLINE search for 1980-98. Using meta-analytical techniques, we assessed the protective effect of breastfeeding according to the age and sex of the infant, the cause of death, and the educational status of the mother. We identified eight studies, data from six of which were available (from Brazil, The Gambia, Ghana, Pakistan, the Philippines, and Senegal). These studies provided information on 1223 deaths of children under two years of age. In the African studies, virtually all babies were breastfed well into the second year of life, making it impossible to include them in the analyses of infant mortality. On the basis of the other three studies, protection provided by breastmilk declined steadily with age during infancy (pooled odds ratios: 5.8 [95% CI 3.4-9.8] for infants <2 months of age, 4.1 [2.7-6.4] for 2-3-month-olds, 2.6 [1.6-3.9] for 4-5-month-olds, 1.8 [1.2-2.8] for 6-8-month-olds, and 1.4 [0.8-2.6] for 9-11-month-olds). In the first 6 months of life, protection against diarrhoea was substantially greater (odds ratio 6.1 [4.1-9.0]) than against deaths due to acute respiratory infections (2.4 [1.6-3.5]). However, for infants aged 6-11 months, similar levels of protection were observed (1.9 [1.2-3.1] and 2.5 [1.4-4.6], respectively). For second-year deaths, the pooled odds ratios from five studies ranged between 1.6 and 2.1. Protection was highest when maternal education was low. These results may help shape policy decisions about feeding choices in the face of the HIV epidemic. Of particular relevance is the need to account for declining levels of protection with age in infancy, the continued protection afforded during the second year of life, and the question of the safety of breastmilk substitutes in families of low socioeconomic status.
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              Detection of replication-competent and pseudotyped human immunodeficiency virus with a sensitive cell line on the basis of activation of an integrated beta-galactosidase gene.

              We have constructed a HeLa cell line that both expresses high levels of CD4 and contains a single integrated copy of a beta-galactosidase gene that is under the control of a truncated human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). This cell line, called CD4-LTR/beta-gal, can be used to determine quantitatively the titer of laboratory-adapted HIV strains, and the method used to do so is as sensitive as the determination of viral titers in a T-cell line by end point dilution. Using this cell line as a titer system, we calculated that HIV-1 stocks contain only one infectious particle per 3,500 to 12,000 virions. Virus derived from a molecular clone of a macrophagetropic provirus will not infect this cell line. We have also cocultivated peripheral blood lymphocyte cultures from HIV-infected individuals with the CD4-LTR/beta-gal indicator cells. In a majority of primary isolates (five of eight), including isolates from asymptomatic patients, rare virus-infected cells that can activate the beta-galactosidase gene are present.
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                Author and article information

                Journal
                Retrovirology
                Retrovirology
                BioMed Central (London )
                1742-4690
                2005
                29 April 2005
                : 2
                : 28
                Affiliations
                [1 ]Department of Microbiology and Immunology, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [2 ]Department of Microbiology and Immunology, Institute for Molecular Medicine and Infectious Diseases, Drexel University, College of Medicine, Philadelphia, Pennsylvania 19104 USA
                [3 ]Department of Neural and Behavioral Sciences, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [4 ]Department of Pediatrics, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [5 ]Department of Pharmacology, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [6 ]Department of Biochemistry, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [7 ]Department of Health Evaluation Sciences, Penn State College of Medicine, Hershey, Pennsylvania 17033 USA
                [8 ]Department of Bioscience and Biotechnology, Drexel University, College of Medicine, Philadelphia, Pennsylvania 19104 USA
                Article
                1742-4690-2-28
                10.1186/1742-4690-2-28
                1097759
                15888210
                dd105649-7bbd-42e0-b6c8-9a3d90e55318
                Copyright © 2005 Urdaneta et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 February 2005
                : 29 April 2005
                Categories
                Research

                Microbiology & Virology
                Microbiology & Virology

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