Press the gourd to float: hepatitis B, hepatitis C co-infection.

Drug source analysis of hepatitis B, hepatitis C transmission path is similar, so the incidence of co-infection is not low.
1-15 per cent of the population is geographically infected with both viruses, significantly increasing the risk of cirrhosis and liver cancer.
both viruses mainly infect liver cells, but the physical fitness and habits of the two are completely different.
B is one of the smallest viruses, a little weak wind, most acute infections will be automatically removed.
even becoming chronic hepatitis B requires years of persistent infection to cause host disease.
but hepatitis B, as a DNA virus, can be compiled into the host genome and can form ring-shaped cccDNA that is very difficult to remove, which is the magic weapon on which it depends.
C is an RNA virus that reproduces only in cell fluids, and antiviral drugs are now available to completely cure hepatitis C infection within 8-12 weeks.
interferon is effective for hepatitis B, hepatitis C treatment, of course, now because sobaldi and other god drugs appear hepatitis C treatment no longer need interferon, but hepatitis B treatment is also highly dependent on interferon.
interferon can not only directly inhibit hepatitis B reproduction, tissue T, B cells besiege hepatitis B infected cells, but also can induce certain DNA modification proteins such as A3A expression and induce cccDNA degradation, which is the only way to cure hepatitis B, so from the point of view of hepatitis B in order to maintain survival should do everything possible to avoid interferon secretion activation.
hepatitis B virus saw hepatitis C into their boarding cell estimates and in the bank shoplifting thin thief suddenly saw a drunk man to rob the bank, the heart secretly thought my life rest.
because shouting hepatitis C virus will attract police interferon, although not necessarily will be caught but the living environment has deteriorated a lot.
treatment of hepatitis C is one of the most successful cases in the history of drug research, with few drugs having a response rate of more than 95%, but hepatitis C therapy now reaches this level in all genotypes.
these therapies are not just about keeping the virus below the detection line, as is the result of AIDS drugs, but about a complete cure.
but hepatitis B co-infection limits this strategy because the reactivation of hepatitis B may be more severe than hepatitis C infection.
to a certain extent hepatitis C to hepatitis B of course human flesh bomb, killing hepatitis C will detonate hepatitis B.
these viruses are only a few thousand base pairs, but their design is exquisite, the complexity of survival strategies is breathtaking.
hepatitis B has become one of the world's largest liver diseases after the cure of hepatitis C, but hepatitis B is mainly distributed in developing countries and is not as important as NASH.
current hepatitis B therapy has a clinical cure rate of only about 10% (i.e., anti-yang), but there is no complete removal of cccDNA therapy.
RNAi technology shows good prospects, but from the results of several smaller clinical trials so far, the Australian anti-yang rate is not more than 20%.
study showed that HCV could theoretically be used as a treatment for hepatitis B, but the strategy of jumping from a fire pit to a puddle paid off, and the HCV virus as a drug had no treatment window.
that while hepatitis C is not the only "drug" that induces interferon, the targeted delivery of HCV is not available in other therapies.
development of liver-targeted delivery interferons may be a strategy, and small molecule drugs that activate TLR, STING, and RIG-1, natural immune system alarms, are also in clinical trials, although these drugs also have systemic toxicity problems.
small molecule drug that only infects liver cells that induce interferon secretion is a 20sible direction.
.