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Scientists from 16 countries have urgedfor exhaustive implementation of cell-culture vaccines in all parts of India tocombat the country’s huge burden ofrabies. At an international meeting inVadodara, India, scientists from theInternational Forum for RabiesPrevention expressed deep concernregarding the use of cheap andhazardous sheep-brain vaccine insteadof safe and effective cell-culturevaccines. India reports at least 20 000rabies deaths a year—the highestnumber of deaths worldwide—and60% of the global fatality from rabies.

Scientists used China and Thailandas examples of countries thatsuccessfully combated rabies bywidespread use of the cell-culturevaccine. The lack of properimplementation of cell-culture vaccineswas blamed for India’s poorperformance in the prevention of rabiesinfection. The continued use of thesheep-brain vaccine despite recom-mendations to phase out the vaccinefrom the Indian Supreme Court (2002)and WHO (1992) was also criticised.

Human cell-culture vaccine doesnot cause adverse effects such as neuritisor encephalitis, which are commonwith the sheep-brain vaccine. WolfgangHaupt (executive director of ChironVaccines, a WHO-endorsed enterpriseand a participant of the forum), saidthat the availability and cost of cell-culture vaccine are no longer a problemfor India due to local production and

financial benefits provided by WHO:“A single dose of the vaccine costs $5 inIndia, while the same costs $120 in theUS and $50 in Europe”.

According to MK Sudarshan(Kempegowda Institute of MedicalSciences, Bangalore, India), whochaired the conference, “someGovernment institutions in India,which produce the sheep-brain vaccine,are expected to cease their productionby December, 2004, following theSupreme Court directions in February2002.” Scientists attending the meetingstressed the need to strengthen theglobal network and spread awareness tocombat this preventable disease. “Weshould work together to control rabiesin Asia and other areas where it isrampant”, said Sudarshan.

However, Salil Kumar Bhattacharya(Calcutta National Medical College,Calcutta, India), highlighted the need totackle increase vaccination of straydogs, the primary vector of rabies inIndia, in addition to the initiation ofnationwide use of cell-culture vaccines.Sanjit Bagchi

Preventable rabies deaths because of wrong vaccine

India dogged by rabies

San

jit B

agch

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Neurology Vol 3 November 2004 http://neurology.thelancet.com

Schwann cells lacking “Cajal” bandselongate more slowly than thedeveloping axons they surround, reportresearchers at Edinburgh University(UK); compensating with more, shorterSchwann cells just slows conductiondown (Nature 2004; 431: 191–95).These findings help throw light on the biology of Charcot-Marie-Tooth(CMT) disease.

Students of neurophysiology learnthat the greater the distance betweenthe nodes of Ranvier, the quicker anervous impulse travels. “But actuallyno-one has ever demonstrated this tobe true”, says team leader PeterBrophy. “These results now show itreally is the case.”

The team compared Schwann-cellelongation and axonal conductionspeed in wild-type mice and a knockoutstrain unable to make the proteinperiaxin. Earlier work showed thatperiaxin forms L-periaxin-dystrophin-related protein 2-dystroglycan (PDG)

complexes in Schwann-cell membranes,and that these are intimately associatedwith the Cajal fibres. “Although theknockout mice produced normalSchwann cells, they could not elongateas fast as the growing axon”, explainsBrophy. “More Schwann cells filled thegaps—increasing the number of nodesof Ranvier and decreasing theinternodal length to about half. Testsshowed the conduction velocities ofthese neurons were down by 50%.”

Periaxin-null Schwann cells mayelongate poorly because of the absenceof Cajal bands. “Ramón y Cajal—whodiscovered these structures around1912—suggested they might have a“nutritional” function. As usual, hewas right because they assist Schwann cell growth”, says Brophy.Immunostaining showed periaxin-null neurons produce poorlydeveloped Cajal bands, perhapsbecause PDG complexes are essentialin their formation. “The Cajal bands

of normal mice had organisedmicrotubule networks around themfrom the nucleus to the paranodes,but those of the null mice, withoutgood Cajal bands, just petered out. Sothe mutant cells could not accumulatemyelin basic protein RNA at theparanodes—something essential inmyelin synthesis”, Brophy explains.

As the knockout mice become olderthey showed severe demyelinationsimilar to that seen in CMT, providing amodel for the disease. The resultssuggest that Cajal bands might bepoorly developed in the Schwann cellsof patients with CMT caused by defectsin the human periaxin gene.

“Unravelling its complete biologywould be a big step towards finding atherapy for this debilitating disease”,says says Adolfo Toledano of theRamón y Cajal Institute, Madrid, Spain,“which may come through knowledgeof the genes involved.”Adrian Burton

Absence of Cajal bands short changes Schwann cells