A brief note on Hepatitis infection

To expand global awareness of Hepatitis, July 28th of every year is considered as ‘World Hepatitis Day’. This day is also the birthday of Dr Baruch Blumberg who was the first person to identify the Hepatitis B virus and subsequently developed a diagnostic test and a vaccine for it. As part of the Hepatitis Day activity, we intend to educate the common people about different types of hepatitis and their preventive measures.

Hepatitis is generally associated with inflammation or enlargement and sometimes dysfunction of the liver and is caused by several viral infections. The infections may be acute (shorter than 6 months) or chronic (longer than 6 months).

Types of Hepatitis Viruses

Six different variants of hepatitis viruses have been identified to date, hepatitis A, B, C, D, E, and G; each differs in disease severity, mode of transmission, and geographical distribution.



Mostly, hepatitis infections are asymptomatic (no detectable symptoms). Acute infection types sometimes exhibit non-specific symptoms like nausea, vomiting, fatigue (extreme tiredness), abnormal appetite, and jaundice. In contrast, the asymptomatic nature of chronic infections keeps the patients as silent carriers. Because of the non-specific symptoms and sometimes asymptomatic nature, it is very difficult to differentiate the type of hepatitis infection. The studies on various types of hepatitis suggest that improved basic sanitation and timely vaccinations can reduce the disease prevalence to a greater extent.


  Structure of hepatitis virus

Similar to other viral structures, the hepatitis virus also has a protein outer coating called nucleocapsid within which a genome is enclosed. Different types of viruses differ in their structural complexity and genome nature.


Infection cycle of Hepatitis in Liver cell

Hepatitis is said to have critical adverse effects on liver health, as it is mostly associated with liver cirrhosis or liver cancer. The disease severity is usually measured clinically by performing liver function tests. Even though the disease is transmitted through body fluids or the digestive tract, the hepatitis viruses can complete their life cycle only in hepatic (liver) cells. So, viral life starts in the human body only once it enters the liver cells. The steps of the viral life cycle in hepatic cells are given below.

1.   Viral assembly on the cell surface: Viral surface proteins detect the specific receptors on the liver cell surface and form an irreversible bond.

2.    Endocytosis: swallowing of the virus into the hepatic cell.

3.  Degradation of core proteins and formation of the naked genome: As our cell’s immune response does not permit foreign proteins inside, viruses degrade their protein outer structure and only genetic material travels within the hepatic cell till it finally reaches the nucleus.

4.     Reverse transcription: Inside the nucleus of the cell, the RNA material of the virus is converted to complementary DNA by a process called reverse transcription. Human cells can produce proteins only from DNA.

5.  Protein synthesis: Viral genome-encoded proteins are produced by two steps - transcription and translation using the cell’s machinery. The cell's replication machinery also produces multiple copies of the viral genome.

6.    Assembly of the viral genome and protein outer coat: The viral genome is enclosed within the outer protein coat by assembling newly transcribed protein molecules.

7.     Exocytosis: The budding and breakage of the plasma membrane; hence, releasing multiple copies of the virus into the bloodstream. Finally, viruses and their components reach excretory systems and spread to other people.


 Hepatitis-associated liver dysfunction

Studies reveal that liver cell damage is caused by the immune responses of the body to the viral load. The activated immune reaction initially leads to inflammation in the infected liver cells and eventually causes cell death. Earlier studies have established a relationship between the liver damage level and the viral load reduction. The healthy liver functions in immunologically compromised patients and newborn babies even after their hepatitis infection can be demonstrated as evidence for the above-explained theory. Such patients act as silent carriers of hepatitis viruses and cause the spreading of the disease involuntarily.

References

1.     https://www.who.int/health-topics/hepatitis#tab=tab_1

2.     https://my.clevelandclinic.org/health/diseases/4245-hepatitis-viral-hepatitis-a-b--c

3.     G. C. TURNER. Hepatitis. British Medical Journal, 1973;1:476-479.

4.     Odenwald M, Paul S. (2022, April 14). Viral hepatitis: Past, present, and future. World Journal of Gastroenterology, 2022; 28(14):1405-1429. Baishideng Publishing Group Inc. https://doi.org/10.3748/wjg.v28.i14.1405

5.     Urban S, Schulze A, Dandri M, Petersen J. The replication cycle of hepatitis B virus. Journal of Hepatology, 2010;52(j):282–284.

6.     Zheng P, Dou Y, Wang Q. Immune response and treatment targets of chronic hepatitis B virus infection: innate and adaptive immunity. Frontiers in Cellular and Infection Microbiology, 2023;13. DOI: 10.3389/fcimb.2023.1206720



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