Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) which is one of the most serious public health problems in the world. Some common approved drugs bring about dose-dependent adverse effects or drug resistance. Therefore, safe and useful new HBV therapeutics are essential. Medicinal plants have particular benefits to treat HBV-infected patients. Traditional medicines have many bioactive compounds that are effective as antiviral candidates including esculetin, helioxanthin, oxymatrine, epigallocatechin-3-gallate, wogonin, alkaloids, polysaccharides, etc. In this chapter, the authors summarize the pathogenesis and protein targets for the treatment of hepatitis B disease. They also indicate several medicinal plants and isolated compounds which are used for preventing and reduce symptoms of this disease.
Top1. Introduction
As stated by WHO, in 2015, the global has over 257 million cases of hepatitis B transmission (Organization, 2017). HBV causes chronic hepatitis, which can progress to cirrhosis, HBV chronic is one of the causes of hepatocellular carcinoma (HCC) (Y. Y. Zhang & Hu, 2015). In Western countries, lingering HBV infection is fairly rare and acquired mainly in a grown-up, whereas in most of Africa and Asia, most infections through blood, from child to child touch in household surroundings, from mother to child (Singh et al., 2017). HBV is considered a neglected tropical diseases (NTDs). Because, first, NTDs mainly influence populations living in subtropical and tropical areas. Second, NTDs cause stigma and discrimination due to disproportionately influence populations living in dearth. Third, by operating public health strategies, NTDs are instantaneously amenable to extensive control, elimination, or extermination. The last, NTDs are moderately neglected by study, resource distribution is not reasonable with the significance of the problem (Lemoine, Eholié, & Lacombe, 2015; O’Hara et al., 2017).
HBV infection for the first time may be asymptomatic, sickness for several days or weeks, or getting sick very quickly. Symptoms may appear after 6 months such as fatigue, loss of appetite, mild fever, nausea, vomiting, joint, muscle aches, dark urine, and yellow skin. Over time, people with chronic HBV can develop symptoms of cirrhosis and liver cancer in 15% - 40% (Harris, 2019).
The pathogenesis of HBV is considered by two factors: the first, the cause of liver hurt is elevated levels of HBV reproduction and infected hepatocytes accumulate viral products. The second, HBV infection may be either straight cytopathic, noncytopathic, or a blend of both in a private patient hang on accumulating viral products (Y. Y. Zhang & Hu, 2015).
Jesse Summers suggested that HBV reproduction in tainted cells had better be controlled due to continued amassing of viral production would lead to injury to the tainted cells. Control of cccDNA (covalently closed circular DNA) amplification is a significant aspect necessary for the possibility of hepadnaviruses to continuously infected cells, devoid of cytopathic effects. He raised the issue that HBV tenacious infection of hepatocytes hangs upon the possibility of virus-related genes to be upheld devoid of cytopathic consequence to the poisoned cells (Summers, Smith, & Horwich, 1990; Summers, Smith, Huang, & Yu, 1991). He showed that the lofty level of viral reproduction and cccDNA duplicate numbers make cytopathic alterations in both the hepatocytes and cell culture of infected animals (Lenhoff & Summers, 1994a, 1994b). HBV reproduction may also distract intracellular organelles, causing ER strain (B. Li et al., 2007) and modification of mitochondrial function (J. Chen & Siddiqui, 2007; Rahmani, Huh, Lasher, & Siddiqui, 2000; Waris, Huh, & Siddiqui, 2001), and raised reproduction may lead to exhaustion of cellular molecular sources like phospholipids which are needed for the creation of cellular coverage, lipoproteins, HBV fraught and subviral particles (Gavilanes, Gonzalez-Ros, & Peterson, 1982; Mohamadkhani et al., 2010; Norton, Gong, Mehta, Lu, & Block, 2003; Peterson, 1981).
Liver damage is also caused by the amassing of viral proteins, without HBV reproduction in hepatocytes. Chisari’s group showed that (1) amassing of the viral consequence in infected cells can happen if the consequence of the viral consequences is beyond the excretion capacity of the master cell or the excretion efficiency is limited by the cellular factors, (2) the amassing of viral consequence can cause a range of main hepatocytic hurt (Chisari et al., 1987), which is similar to the histopathological modifications described in hepatitis B.
Master cells can limit viral reproduction by adjusting entrance to cellular factors and structure demanded reproduction or throughout cellular factors that are naturally opposed to stairs in the HBV lifecycle. As a result, when assessing HBV-mediated cytopathic influence, the effect of cellular limit on HBV reproduction should also be inspected. It is supposed that HBV infection can lead to either straight cytopathic or non-cytopathic effects hang on modifications of the intracellular limit on viral replication (Y. Y. Zhang & Hu, 2015).