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High treatment rates delay effect of HIV on tuberculosis
Newsdesk High treatment rates delay effect of HIV on tuberculosis Very high tuberculosis treatment rates in developing countries could bring the tuberculosis epidemics in these countries under control even in the presence of HIV epidemics (J Acquir Immune Defic Syndr 2001; 28: 437–44). “Our work is the first to quantify the effect of HIV epidemics on tuberculosis outbreaks and to show how high tuberculosis treatment rates could actually halt this synergistic effect”, lead investigator Sally Blower (University of California, Los Angeles, CA, USA) told TLID. To predict the “probability and average expected outbreak size that would be generated in a 2-year period from a single index case of [untreated] infectious tuberculosis”, Blower and colleagues used a model in which population tuberculosis treatment rates were varied from 0% to 100%; prevalence of HIV and mixed patterns of the HIV and the
tuberculosis epidemics were also independently varied. The researchers found that in places with effective tuberculosis control programmes, such as San Francisco in the USA, HIV epidemics are less likely to increase the number or size of tuberculosis outbreaks. By contrast, in places with low or moderate tuberculosis treatment rates, as is the case in most developing countries, “even a modest HIV epidemic could nearly double the size of tuberculosis outbreaks”. The authors caution that because the WHO’s calculations for global treatment rates did not include HIV’s amplification effect on tuberculosis, they grossly underestimate treatment levels necessary for global control of drug-resistant tuberculosis. The team recommends a significant increase in tuberculosis treatment target rates for countries with high prevalence of both tuberculosis and HIV.
But Paul Nunn of WHO’s Stop TB programme disagrees, saying that because the research deals with the tuberculosis situation in low-prevalence countries, it does not calculate the impact of HIV on tuberculosis incidence in countries where tuberculosis prevalence is high and the disease is endemic. Nevertheless, “it provides nice intellectual support for the observations made in dozens of highHIV-prevalence African countries that tuberculosis rates can rise, even as high as five-fold, as HIV increases”, he notes. Nunn adds: “The important question is—what is the correct public-health response to such increases in tuberculosis? An expanded scope of interventions is probably needed rather than just trying to maximise treatment rates.” Khabir Ahmad
New way to knock pneumococcus?
THE LANCET Infectious Diseases Vol 2 February 2002
http://infection.thelancet.com
of pneumococcal cells and the consequent spillage of compounds that degrade host endothelium and epithelium. The team were thus able to build the first three-dimensional pictures of the choline-binding domain. The structure, a left-handed -3-solenoid spiral staircase made of stacked -hairpins forming a superhelix, is new to science. “Knowing this could help us design compounds that knock ChPBs off the cell wall, opening up a route towards new drugs against pneumonia and other pneumococcus pathologies”, says Fernández-Tornero. Guillermo Gimenez-Gallego, co-author and team leader adds, “Given the high homology between the choline binding domains of pneumococcal ChPBs and those now known in other bacteria, any such drug might be useful against them too”. ChBPs have recently been discovered in Clostridium difficile, Clostridium perfringens, Streptococcus mutans, and Streptococcus downei. Guillermo Gimenez
Spanish scientists have unravelled the domain—a stretch of the protein that structure of the molecular domain that latches non-covalently onto choline binds virulence proteins to the cell moieties in teichoic and lipoteichoic wall of pneumococcus (Streptococcus acids in the bacterial cell wall. Attack pneumoniae), raising hopes that new the binding domains and the ChPBs drugs can be designed to combat the might be lost, rendering the bacterium pathogen (Nat Struct Biol 2001; 8: virtually harmless. 1020–24). Antibiotic-resistant strains are common in Spain where penicillin is of no use in 80% of infections. Although a vaccine exists, it is ineffective in children under 2 years of age and provides protection in only 50% of adults. A new way to fight back may be in the pipeline, however, thanks to the elucidation of the structure of the binding domain that fastens virulence-determining proteins to the bacterial cell wall. Essential in many of the steps required to Three-dimensional model of the choline-binding site. infect a host—eg, adhesion to host Carlos Fernández-Tornero and cells, nasopharyngeal colonisation, Rubens López and associates at the or invasion of the bloodstream—15 Biological Research Centre, Madrid, types of these so-called cholinesolved the structure of crystallised binding proteins (ChBPs) are known. pneumococcal autolysin (LytA), a Common to all serotypes, most stick to ChBP responsible for the autolysis the bacterium via a highly conserved
Adrian Burton
65
For personal use. Only reproduce with permission from The Lancet Publishing Group.
tuberculosis epidemics were also independently varied. The researchers found that in places with effective tuberculosis control programmes, such as San Francisco in the USA, HIV epidemics are less likely to increase the number or size of tuberculosis outbreaks. By contrast, in places with low or moderate tuberculosis treatment rates, as is the case in most developing countries, “even a modest HIV epidemic could nearly double the size of tuberculosis outbreaks”. The authors caution that because the WHO’s calculations for global treatment rates did not include HIV’s amplification effect on tuberculosis, they grossly underestimate treatment levels necessary for global control of drug-resistant tuberculosis. The team recommends a significant increase in tuberculosis treatment target rates for countries with high prevalence of both tuberculosis and HIV.
But Paul Nunn of WHO’s Stop TB programme disagrees, saying that because the research deals with the tuberculosis situation in low-prevalence countries, it does not calculate the impact of HIV on tuberculosis incidence in countries where tuberculosis prevalence is high and the disease is endemic. Nevertheless, “it provides nice intellectual support for the observations made in dozens of highHIV-prevalence African countries that tuberculosis rates can rise, even as high as five-fold, as HIV increases”, he notes. Nunn adds: “The important question is—what is the correct public-health response to such increases in tuberculosis? An expanded scope of interventions is probably needed rather than just trying to maximise treatment rates.” Khabir Ahmad
New way to knock pneumococcus?
THE LANCET Infectious Diseases Vol 2 February 2002
http://infection.thelancet.com
of pneumococcal cells and the consequent spillage of compounds that degrade host endothelium and epithelium. The team were thus able to build the first three-dimensional pictures of the choline-binding domain. The structure, a left-handed -3-solenoid spiral staircase made of stacked -hairpins forming a superhelix, is new to science. “Knowing this could help us design compounds that knock ChPBs off the cell wall, opening up a route towards new drugs against pneumonia and other pneumococcus pathologies”, says Fernández-Tornero. Guillermo Gimenez-Gallego, co-author and team leader adds, “Given the high homology between the choline binding domains of pneumococcal ChPBs and those now known in other bacteria, any such drug might be useful against them too”. ChBPs have recently been discovered in Clostridium difficile, Clostridium perfringens, Streptococcus mutans, and Streptococcus downei. Guillermo Gimenez
Spanish scientists have unravelled the domain—a stretch of the protein that structure of the molecular domain that latches non-covalently onto choline binds virulence proteins to the cell moieties in teichoic and lipoteichoic wall of pneumococcus (Streptococcus acids in the bacterial cell wall. Attack pneumoniae), raising hopes that new the binding domains and the ChPBs drugs can be designed to combat the might be lost, rendering the bacterium pathogen (Nat Struct Biol 2001; 8: virtually harmless. 1020–24). Antibiotic-resistant strains are common in Spain where penicillin is of no use in 80% of infections. Although a vaccine exists, it is ineffective in children under 2 years of age and provides protection in only 50% of adults. A new way to fight back may be in the pipeline, however, thanks to the elucidation of the structure of the binding domain that fastens virulence-determining proteins to the bacterial cell wall. Essential in many of the steps required to Three-dimensional model of the choline-binding site. infect a host—eg, adhesion to host Carlos Fernández-Tornero and cells, nasopharyngeal colonisation, Rubens López and associates at the or invasion of the bloodstream—15 Biological Research Centre, Madrid, types of these so-called cholinesolved the structure of crystallised binding proteins (ChBPs) are known. pneumococcal autolysin (LytA), a Common to all serotypes, most stick to ChBP responsible for the autolysis the bacterium via a highly conserved
Adrian Burton
65
For personal use. Only reproduce with permission from The Lancet Publishing Group.