This virus has a wide geographic distribution, circulating in Africa, the Middle East, Asia, and Central and South-Eastern Europe2. was found out to be much like a computer virus isolated in 1956 in Congo3. Based on the serosurvey data, the presence of CCHF was suspected long back in Jammu and Kashmir in India; similarly CCHF reactive antibodies were recognized in southern India4,5. The presence of this computer virus (CCHFV) was confirmed for the first time during investigation of a nosocomial outbreak in Ahmadabad, Gujarat State, India in 20116,7. This CCHF outbreak resulted in four deaths in 2011. The National Institute of Virology (NIV), Pune, found evidence of this computer virus causing viral haemorrhagic fever instances in humans during 2010 in Rajkot, Gujarat, India6,7. The analysis of these instances was performed by real-time opposite transcriptase (RT)-PCR or IgM and/or IgG positivity by enzyme linked immunosorbent assay (ELISA). A serosurvey in home animals before and after the outbreak ITGB2 exposed the presence of CCHFV specific IgG antibodies and viral RNA7. This computer virus was also isolated fromHyalomma anatolicum anatolicumticks from your Kolat Gefitinib (Iressa) town, Sanand Taluka, Ahmadabad, Gujarat, of index case. State government experienced taken initiatives to track the instances and reduce the tick populace. After the nosocomial outbreak in January 2011, again one more suspected human being case was confirmed positive for CCHFV by Gefitinib (Iressa) qRT-PCR and RT-PCR in May 2011. This case experienced similar clinical demonstration as described earlier7. Here we statement a fatal case of CCHF from Ahmadabad, Gujarat on June 21, 2012. A physician, 29 12 months aged male was admitted on June 20, 2012 in Vadilal Sarabhai Hospital, Ahmadabad, Gujarat with issues of fever, headache, anorexia, general weakness, metallic taste in mouth since last two days. The patient experienced no symptom suggestive of sensitive condition, diabetes, but experienced past history of hepatitis E computer virus illness about one and half 12 months ago. Personal history exposed that he was vegetarian, having no habit of smoking, alcohol, drugs and tobacco consumption. Exposure history also exposed that he had an accidental contact (splash of infected blood in his eyes) with the index patient. This physician experienced treated the index case, resident of Kochariya town of Bawla Taluka, Ahmadabad, Gujarat, who experienced related sign of haemorrhagic fever and died a week earlier. Cardiovascular system exam was normal, individual was conscious, oriented, no musculoskeletal deformities were observed. Haemorrhagic manifestations included black coloured loose stool. Decrease in platelet counts (32,000 /l), improved levels of prothrombin time, activated partial thromboplastin time (17.5 & 31.7 sec), and ferritin up to 2928.9 ng/ml indicated severe malfunction of blood coagulating factors. The improved levels of aspartate transaminase (SGOT, 154.8 U/l), alanine transaminase Gefitinib (Iressa) (SGPT, 132.7 U/l) and lactate dehydrogenase (1152.3 U/l) suggested liver dysfunction. Clinicopathological findings were suggestive of viral haemorrhagic fever; hence, the clinical sample was sent to NIV, Pune, for investigation, especially for CCHFV testing. Supportive therapy given to the patient during the course of the disease consisted of hydration, antibiotics and control of heat. Blood transfusions, two plasma and four platelets solutions were transfused. Despite the treatment, the medical Gefitinib (Iressa) features deteriorated and the patient died on June 22 due to haemorrhagic shock and vital organ failure. After the death of the index case, a few tick swimming pools, and blood and serum samples of livestock were collected from the house of index case by the Animal Husbandry Division, Gujarat and sent to NIV, Pune, for investigation for CCHFV. After this case, to ascertain whether CCHFV infections had occurred in contacts (hospital staff), an additional suspected six blood samples were received for the screening of viral haemorrhagic fever. The medical samples (serum and plasma) of medical professional (human being case-A), tick pool (n=1) and animal samples (n=14) and suspected contact human samples (n=6) were screened by real-time RT-PCR and nested RT-PCR specific to CCHFV based on nucleocapsid gene8,9. Real-time RT-PCR data showed presence of high titre computer virus [threshold cycle (Ct)=18] in case-A and also RT-PCR positivity. Of the 14 animal samples (8 calf and 6 adult cow), only one calf sample was found positive for CCHFV in real-time RT-PCR (Ct= 36) and also in nested RT-PCR. Tick pool (n=1) was also found to be bad by RT-PCR. The suspected six human being samples were found to be bad for CCHFV by real time RT-PCR. After confirmation of short fragment as CCHFV, total S gene was amplified and sequenced from medical specimen of case A by a single step RT-PCR (NIV unpublished data). Blast analysis showed homology of 99.0 and 98.0 per cent with Tajikistan sequencesAY049083andAY297691. This sequence showed 99.8 per cent homology with Indian CCHFV sequences from outbreak of 20117. The S section sequence of case-A was analyzed with earlier CCHF outbreak sequence from India, it showed that this sequence clustered in Indian group.