extramarital sexual activities (2.4%), tattooing (3.6%) were found to be independent risk factors of being HCVpositive. No apparent risk factors could be demonstrated in 29 (11.2%) of the positive cases. CONCLUSION:Our data indicate that a history of transfusion and iv drug abuse and haemodialysis are important risk factors for HCV infection in our area and that more careful pretransfusion screening of blood for anti-HCV must be introduced in our blood banks. Improvements in certain lifestyle patterns, and customs in this area may be essential to prevent transmission of the infection. INTRODUCTIONHepatitis C virus (HCV) infection is responsible for considerable morbidity and mortality worldwide. HCV is a leading cause of liver failure and liver transplantation in adults. Identified risk factors for HCV infection include intravenous (IV) drug use, exposure to infected blood products, and intranasal drug use [1] . High-risk sexual activity [multiple sexual partners, history of sexually transmitted disease (STD)], tattooing, and skin piercing have also been suggested to be associated with increased risk for HCV [2] . In addition, mother-to-infant transmission has been demonstrated [3,4] , but the possibility of other transmission routes has not been thoroughly explored. With the use of RT-PCR or bDNA techniques, HCVRNA has been detected in many systemic fluids other than blood, including peritoneal fluids, seminal and vaginal secretion, urine, and feces. These observations, however, have not been confirmed by all investigators [5] . The possibility of HCV replication in the mosquito alimentary tract has recently been demonstrated, but the epidemiological importance of this has not yet been RAPID COMMUNICATION Seroepidemiology of hepatitis C and its risk factors in

Hypothyroidism has a gradual onset and non-specific symptoms, which might be subtle, and which might therefore be ignored or misdiagnosed. Subclinical hypothyroidism is a well-established phenomenon where a patient does not have thyroid symptoms, but shows biochemical evidences of hypothyroidism. However, diagnosis and treatment of these patients may prevent development of overt hypothyroidism and cardiovascular symptoms. Replacement therapy with levothyroxine (T4) is the treatment of choice for hypothyroidism; levothyroxine is taken daily, provides stable plasma levels and is suitable for the majority of patients. Patients with certain forms of hypothyroidism -central hypothyroidism, thyroidectomy patients and patients with "low T3 syndrome" -may benefit from treatment with liothyronine (T3), which is more potent and has a shorter onset of action. The use of liothyronine in combination with levothyroxine is controversial, but there is evidence that some patients, particularly those with deiodinase 2 and thyroid hormone transporter expression polymorphisms, may benefit from combination therapy.

The neuronal ceroid lipofuscinoses (NCLs), more commonly referred to as Batten disease, are a group of inherited lysosomal storage disorders that present with neurodegeneration, loss of vision and premature death. There are at least 13 genetically distinct forms of NCL. Enzyme replacement therapies and preclinical studies on gene supplementation have shown promising results for NCLs caused by lysosomal enzyme deficiencies. The development of gene therapies targeting the brain for NCLs caused by defects in transmembrane proteins has been more challenging and only limited therapeutic effects in animal models have been achieved so far. Here, we describe the development of an adeno-associated virus (AAV)-mediated gene therapy to treat the neurodegeneration in a mouse model of CLN6 disease, a form of NCL with a deficiency in the membrane-bound protein CLN6. We show that neonatal bilateral intracerebroventricular injections with AAV9 carrying CLN6 increase lifespan by more than 90%, maintain motor skills and motor coordination and reduce neuropathological hallmarks of Cln6-deficient mice up to 23 months post vector administration. These data demonstrate that brain-directed gene therapy is a valid strategy to treat the neurodegeneration of CLN6 disease and may be applied to other forms of NCL caused by transmembrane protein deficiencies in the future.