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The hepatitis C virus affects people in different ways and has several stages: Incubation period. This is the time between first exposure to the start of the disease. It can last anywhere from 14 to 80 days, but the average is 45. Acute hepatitis C. This is a short-term illness that lasts for the ...
Now that you know how you get hepatitis C, you can take steps to protect yourself from the virus. For instance: Avoid sharing needles or other paraphernalia related to intravenous drugs. Wear ...
Spiderlike blood vessels on your skin (spider angiomas) Every chronic hepatitis C infection starts with an acute phase. Acute hepatitis C usually goes undiagnosed because it rarely causes symptoms. When signs and symptoms are present, they may include jaundice, along with fatigue, nausea, fever and muscle aches.
You increase your risk for contracting hepatitis C if you: have sex without condoms with more than one sexual partner have a sexually transmitted disease or HIV engage in sexual activity that could cause bleeding
Hepatitis C is a blood-borne virus, meaning that a person must come into contact with blood that contains the virus to contract it. Most new cases of hepatitis C in the U.S. are due to injecting...
Hepatitis C is spread through exposure to infected blood. Intravenous drug abuse with the use of contaminated, shared needles is the most common mode of transmission. The risk of acquiring hepatitis C through sexual contact or breastfeeding is very low.
The Hepatitis C virus internal ribosome entry site, or HCV IRES, is an RNA structure within the 5'UTR of the HCV genome that mediates cap-independent translation initiation. Protein translation of most eukaryotic mRNAs occurs by a cap-dependent mechanism and requires association of Met-tRNAiMet, several eukaryotic initiation factors, and GTP with the 40S ribosomal subunit, recruitment to the 5' cap, and scanning along the 5' UTR to reach to start codon. In contrast, translation of hepatitis C virus (HCV) mRNA is initiated by a different mechanism from the usual 5' cap-binding model. This alternate mechanism relies on the direct binding of the 40S ribosomal subunit by the internal ribosome entry site (IRES) in the 5' UTR of HCV RNA. The HCV IRES adopts a complex structure, and may differ significantly from IRES elements identified in picornaviruses. A small number of eukaryotic mRNA have been shown to be translated by internal ribosome entry.
HCV genomeE1 is one of two subunits of the envelope glycoprotein found in the hepatitis C virus. The other subunit is E2. This protein is a type 1 transmembrane protein with a highly glycosylated N-terminal ectodomain and a C-terminal hydrophobic anchor. After being synthesized the E1 glycoproteins associates with the E2 glycoprotein as a noncovalent heterodimer.