What is a Virus and Virology

WHAT HAPPENS AT FIRST CONTACT WITH A VIRUS?

Nature has equipped the human body with many layers of protection against intruders or foreign bodies before getting to the blood stream and activating the immune system. These include the skin and the mucus membranes that line the mouth, ear, private parts, nostrils, lungs, the eyes and the digestive tract. These membranes secrete antimicrobial agents that encounter microbes before they get into the blood stream. It is the breakdown in one or all of these defenses that lead to encounters with the immune system. These encounters are first picked up by the sensors nature puts in place to alarm the immune system (like a home alarm system). When the immune system encounters an intruder(like the home security system), its sensors triggers the alarm system that activates chemical messengers to attack the intruders-a protective mechanism(This is likened to the alarm monitoring company sending police men to the encounter i.e. the intruder.

Oxidative and Cellular Responses during Viral Infection

The cellular immune responses include the actions of chemical messengers called leukotrines and prostaglandins. Prostaglandins open the blood vessels for white blood cells to flow in and initiate the healing process. They also send pain messages to the brain by stimulating nerve endings.  Leukotrines, like the joint chief of staff, directs the activities of white blood cells at the site of infection. They orchestrate increased migration of white blood cells to the liver, where they filter intruders out of the blood while trying to restore homeostasis and normality. These migratory patterns are responsible for the warmth, heat, pain and redness experienced during inflammation.

How the Liver Encounter Viral and Antigenic Attacks

Under the direction of the leukotrines, kupffer cells (specialized liver cells) are the first to engage an invading virus. Kupffer cells serve as first responders or body guards in the liver.  They are responsible for scouting the liver for intruders such as the hepatitis virus. On contact with the hepatitis virus, they hold down the virus, break it into fragments, and signal the regulators of the immune system, the T lymphocytes (Schmidt, Smith and Sehnert, 1994).  After T-lymphocytes are signaled for help, T –helper cells bind to the kupffer cells and they lock onto viral antigens to form antigen-antibody complexes and interact with other subtypes of the T- cells to fight the invading virus. Other T-helper cells rush to the spleen and the lymph nodes for more T-helper cells to keep up the tempo while soliciting the immune system for other reinforcements.

The activities of the T-cells

The activated T-helper cells again stimulate the production and multiplication of other specialized types of T-cells called the T–killer cells, which attack the virus at the site of infection and kill infected host cells. The T- killer cells kill the host cells, infected by the Hepatitis, by puncturing their membranes and letting the viral contents spill out hence hindering their usage for viral replication (Schmidt, Smith and Sehnert, 1994).

The activated T-helper cells also stimulate the production of B-cells that reside in the spleen which manufacture antibodies to destroy the virus. Meanwhile, under the actions of the leukotrines, interferons are produced which make the host cells, infected by the Hepatitis virus, self destruct - nature’s way of stopping the spread of infections.

When the Immune system is Sluggish during Viral Infection?

In individuals whose immune or lymphatic  system are sluggish due to malnutrition or stress, the immune cells fail to launch the above defenses and the invading viruses use the host’s genetic material to replicate themselves. In humans with good immune or lymphatic systems, the infection manifest only the acute phase and is localized to a part of the body manifesting as style, crypt, scar  or carbuncle after acute reactions to the invader. These responses deactivate the alarm and the war dwindles signifying recovery –happy face!!!!!Hurray!!!!!.

As the war dwindles, the T-helper cells again send out the suppressor T-cells, a third type of the T-cells, to slow down or stop the activity of the B–cells and T–killer cells i.e. calling a truce .They stop the attack in acute infections and give room for recovery. The memory cells are produced by the first exposure to infective agents. They stay in the blood stream for years and give lifelong immunity from subsequent infections and increase response time to invasion by the same virus (Schmidt, Smith and Sehnert, 1994).

Putting all the blame on the virus and combating hepatitis exclusively with antiviral is like making an accessory to a crime the prime suspect. An aberrant virus, fungus or bacteria in the body can only survive in an acidic environment (Baroody, 2002).
‘Currently, the FDA has not approved viral count as a diagnostic procedure; therefore it is only used for research purposes .The procedures for viral count is very variable depending on the specific lab which performed the test. Different labs at different times almost always produce different results. Viral counts can change within a day or within a week. Efforts aimed at eliminating the virus at the cost of the patient’s health are only short term. Along these improvements is deterioration of life. While synthetic Alpha interferon, Reberton and anti-virals improve the lab markers and liver function tests, patients become sicker and weaker and their quality of life deteriorate’ says Quigcai Zhang of the Zhang Clinic.

It is the failure and breakdown of this process and the immune-lymphatic system that made hepatitis virus attack infective and chronic.

WHAT ARE OXIDATIVE RESPONSES DURING VIRAL INFECTION?

The oxidative phase involves the movement (leakage) of fluids, antibodies and blood plasma, from the blood vessels to the surrounding tissues which ultimately leads to swelling around the liver. The liver (like jello) does not experience pain or discomfort. The swelling distends the surrounding tissues, compress, irritate and stimulate their nerve endings causing the pain experienced during inflammation. Normally this process is self limiting and the individual may or may not experience minor symptoms of nausea, fever, vomiting or mild scar.

WHAT HAPPENS WHEN THE INFECTION BECOMES CHRONIC?

In chronic inflammatory liver disease, this process refuses to stop; the liver becomes a battle field like a California brush fire that spreads uncontrollably. In individuals with under active immune system the alarm system fails to respond to the invader. Similarly in cases of chronic inflammatory diseases, the alarm goes on and on initiating excessive responses that harm the host. Both of these scenarios constitute inappropriate responses of nature’s war arsenal against pathogens and the host is caught in a cross-fire. Instead of the alarm company sending police men to encounter the intruder, an apache helicopter is sent to encounter the intruder. The damage caused by excessive response of the immune system further weakens the liver cells making it possible for the invading virus to take advantage of this venerability and replicate uncontrollably. It is like a friend becoming an arsonist.

HOW’S THE LIVER DAMAGED DURING VIRAL INFECTION?

During chronic inflammation, the liver often suffers from the friendly fires from these healing messengers that are directed at the pathogen (virus).  The efforts directed by the white blood cells to counteract the virus, end up on the liver (like aiming for the moon and hitting the stars). The responses from the immune system ultimately cause the damage associated with Hepatitis and the disruptions in the functions of the liver are elicited as the symptoms of Hepatitis that includes elevated liver enzymes. This leaves localized scar tissues on the liver. If this continues unabated, scar tissues reduces the functional area and abilities of the liver. The scar is referred to as cirrhosis. If the inflammatory fires are not abated, liver cancer ensures.  The driving force in chronic hepatitis is the ability of the virus to break through the host immune defenses or weak cellular defenses and excessive immunological response or friendly fires that causes cirrhosis.