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IN THE NAME OF GOD

IN THE NAME OF GOD. Crimean–Congo Hemorrhagic Fever virus Producer : Azam Izadi. History of Crimean–Congo hemorrhagic fever. CCHF was described by a physician in the 12th century from the region that is presently Tadzhikistan . Hemorrhagic disease with the presence of blood in: Urine

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IN THE NAME OF GOD

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  1. IN THE NAME OF GOD

  2. Crimean–Congo Hemorrhagic Fever virusProducer : AzamIzadi

  3. History of Crimean–Congo hemorrhagic fever • CCHF was described by a physician in the 12th century from the region that is presently Tadzhikistan. • Hemorrhagic disease with the presence of blood in: • Urine • Vomitus • Gums • Sputum • Abdominal cavity • Caused by a tick

  4. CCHF had three names in southern Uzbekistan: • khungribta (blood taking) • Khunymuny(nose bleeding) • karakhalak (black death)

  5. Discovery of virus: • CHF came to the attention of modern medical science in 1944–1945 when about 200 Soviet military personnel were infected during an epidemic in war-torn Crimea. • Virus isolated from a patient in Congo in 1956

  6. In 1967a breakthrough in CHF research came when Chumakov at the Institute of Poliomyelitis in Moscow first used newborn white micefor CHF virus isolation. This now gave researchers an actual virus for production of the necessary reagents needed forserologicalsurveys.

  7. Classification of virus: CCHFV is a member of the Nairovirusgenusof the family Bunyaviridae. There are seven recognized species in the genus Nairovirus containing34viralstrains

  8. Structure of virus: Virions are spherical Helicalnucleocapsid Approximately 100 nm in diameter Lipid bilayered envelope approximately 5–7 nm thick Glycoprotein spikes 8–10 nm in length

  9. Contain three structural proteins: Twoenvelope glycoproteins G2 and G1 Nucleocapsid protein (N)

  10. Genome of virus The genome is composed of three negative-strand RNA segments: S, M, and L.(11-19 kb) S encoding N nucleocapsid M encoding G2 and G1 glycoproteinsLencodingL polymerase

  11. The three RNA genome segments (S, M, and L) are complexed with nucleocapsid protein to form ribonucleocapsidstructures. The nucleocapsids and RNA dependent RNA polymeraseare packaged within a lipid envelope that contains the viral glycoproteins G1 and G2.

  12. Replication of virus: 1. attachment of virions to cell-surface receptors 2. entry via endocytosis followed by membrane fusion 3. primary transcription (Transcription of negative sense vRNA to mRNA) 4. translation of viral proteins

  13. Translation : • L and S segments of mRNA are translated on free ribosomes in cytoplasm • M segment mRNA is translated on ER-bound ribosomes

  14. 5.replication of vRNA via a cRNAintermediate vRNA is used as a template by viral polymerase to make cRNA cRNA is used as a template to make more negative sense strands ofvRNA

  15. 6.assembly of virions at the Golgi or plasma membrane 7. egress by budding into the Golgi followed by exocytosis, or budding through the plasma membrane.

  16. Replication cycle

  17. Tick vectors: CCHFV has been isolated from at least 31species of ticks. The biological role of ticks is also important, not only as virus vectors, but also as reservoirs of the virus in nature. Hyalommaanatolicumticksa common CCHFVvector .

  18. Vertebrate reservoir hosts: • Isolated from numerous domestic and wild vertebrates, including: -Goats -Sheep -Hares -Mouse -Domestic dogs -Horses -Donkeys

  19. After experimental inoculation of birds with CCHFV, they remained healthy. Birds appear to be refractory to CCHF viremia. In 1984, a case of CCHF occurred in a worker who became ill after slaughtering ostriches on a farm in South Africa.

  20. tick–vertebrate–tick cycle

  21. How is the disease transmitted to humans? - Congo fever is transmissible to humans through contact with infected blood, other tissue or a tick bite. -People handling livestock or ostriches during routine procedures, such as vaccinations or slaughtering of animals, are at risk. -People can also get infected through the handling of ticks.

  22. Four distinct phases: 1- Incubation:the incubation period after a tick bite can be as short as 1–3 days, but can much longer. 2-Prehemorrhagic: Sudden fever(39-41◦C) , 5-12 days Chills Headache Dizziness Photophobia Abdominal pains, vomiting, diarrhea Brady cardia, low blood pressure .

  23. 3-Hemorrhagic: In severe cases, 3–6 days after onset of disease: • The virus attacks and destroys blood vessels. • The red rash, first appears on the whites of the eyes, roof of the mouth, throat and skin. this rash spreads and bleeding from the bowel. • Petechiae and ecchymosis

  24. Bleeding from: Nose Gums Vagina Blood in the urine Vomitus and tar-like stools resulting from intestinal hemorrhages. In severe cases, the haemorrhaging causes major organs - such as the liver, kidneys and lungs - to fail.

  25. 4-Convalescence:it begins about 15–20 days after onset of illness • Weak pulse • Sometimes completeloss of hair • Headache, dizziness, nausea • Poor appetite, poor vision • Loss of hearing, and loss of memory • These problems are rarely permanent, but may persist for a year or more.

  26. Fever Headache Sore throat General malaise Muscle aches Sore eyes, including light sensitivity. Red rash on the eyes, roof of the mouth and skin, caused by haemorrhaging of tiny blood vessels. Symptoms:

  27. Nosebleeding Bleeding gums Nausea Loss of appetite Vomiting Diarrhoea Chest pain Dizziness Seizures Death

  28. Antibody Response in CCHF: IgG and IgM antibodies became demonstrable by indirect immunofluorescenceon days 7 to 9 of illness Maximum titers of antibody were usually attained in the second to third week of illness. Titers of IgM declined gradually and were low or negative by the fourth month. .

  29. In some patients titers of IgG increased markedly between 2 and 4 months after onset of illness and remained demonstrable by indirect immunofluorescence3 years after infection. Techniques for demonstrating antibody were: indirect immunofluorescence complement-fixation immunodiffusion

  30. CCHF : laboratory diagnosis Viral detection: (bloodspecimen) -RT-PCR - Cell culture Antibodydetection : (serumsample) • IFA • ELISA

  31. VACCINE: An inactivated suckling mouse brain vaccine was developed in the Soviet Union in 1960. Brain tissue suspensions were inactivated by formaldehyde and heat treatment to obtain safe. The efficacy of the vaccine was tested using the complement fixation (CF) technique.

  32. The vaccine has been used for high risk groups in Bulgaria since 1974. There are concerns about using mouse brain vaccine because of possible autoimmune responses. . Modern vaccines are DNA vaccines, recombinant viral protein-based vaccines. American scientists have developed a DNA vaccine containingthe CCHFV genome M segment.

  33. How can people at risk be protected against CCHF? • Many human infections result by tick bites: - Animals should be treated with acaricides to reduce the numberof ticks. - Clothing can be treated with acaricides. • People coming into contact with fresh blood are at risk: - Protective clothing should be worn

  34. Prevention strategies • Avoid travelling to regions where CCHF is endemic. • Wear long trousers, long socks and boots when outdoors. • Use insect repellent on all areas of exposed skin. • Avoid touching animals or, if you must, wear gloves and other protective clothing. • If you find a tick on your skin, Use tweezers to grasp the tick’s head, then pull the tick out of your skin, don’t squeeze the tick’s body.

  35. TREATMENT: Ribavirin: • The efficacy of ribavirin againstCCHFV was first described in vitro in 1989. • Ribavirin is a purine nucleoside analogue with broad-spectrumantiviral activity.

  36. A recent study confirmed that ribavirin inhibitedCCHFV replication . • In a study in suckling miceusing the ribavirin significantlyreducedviral replication in the liver and prevented infection of brain andheart tissues.

  37. WITH RIBAVIRIN: • Higher survival rates • Shorter recovery time • Earlier return to normal levels of laboratory parameters

  38. CCHFV possesses mechanisms to defeat the interferon-induced defense mechanisms by delaying IFN secretion for 48 hours post-infection. Recombinant interferons exhibit activity against CCHFV in vitro

  39. Mortality rate: -The average mortality rate is 30–50% -However, rates ashigh as 72.7% and 80% have been reported from the UnitedArab Emirates and China.

  40. BIOTERORISM: CCHFV might be used as an agent of bioterrorism or biowarfare. CCHFV can be transmitted from personto person, has a high case-fatality rate.

  41. Geographical distribution There are reports of viral isolation and disease from more than 30countries in Africa, Asia, southeast Europe.

  42. Turkey has experienced the largest ever recorded CCHF outbreak with more than 4,400 confirmed cases mainly from rural areas.

  43. CCHF in IRAN: 610 cases have been reported in Zahedan 100 cases have been reported in Khorasan

  44. References1-Whitehouse ,C.,(2004), Crimean–Congo hemorrhagic fever,Crimean–Congo fever, Antiviral Research,64:145-160 2- Paragas,J. Whitehouse,C. Endy,T. Bray,M.,(2004),A simple assay for determining antiviral activity against Crimean-Congo hemorrhagic fever virus, Antiviral Research,62:21-25 3-Samudzia,R. Lemanb, P. Paweskab,J. Swanepoelb,R. Burta,F.,(2012), Bacterial expression of Crimean-Congo hemorrhagic fever virus nucleoprotein, Journal of Virological Methods ,179:70-76 4-Shepherd,J.Swanepoel,R.Leman,A., (1989),Antibody Response in Crimean-Congo Hemorrhagic Fever,Clin Infect Dis,11:801-806 5- Keshtkar,M. ,Kuhnb,J. Christovac,I. Bradfuted,B.,(2011), Crimean-Congo hemorrhagic fever: Current and future prospects of vaccines and therapies, Antiviral Research ,90:85-92

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