1 About Infectious Disease

Reading 3

Ebola and Measles: Ecology and Biology

The purpose of this reading is to give students a better grasp of the ecology and biology of the Ebola and Measles viruses.

This reading will provide you with additional information on the ecology and biology of two viruses that have risen to increased prominence recently — Ebola and Measles.

I. Infectious diseases – Ebola and Measles viruses

In the beginning of your exploration of infectious diseases and their causes, you read stories about two recent epidemics, one of an emerging disease (i.e., a disease that has appeared in a population for the first time, or that may have existed previously but is rapidly increasing in incidence or geographic range) and another about a re-emerging disease (i.e., a disease that had decreased in incidence in the global population as a result of public health policies and vaccination but has had a resurgence as a public health problem).
Ebola Virus Disease, caused by the Ebola virus is an example of an emerging disease; measles (also known as Rubeola) caused by the measles virus is an example of a re-emerging disease. Although the symptoms and the degree of contagiousness (how readily the virus can spread) of the two diseases are very different, the viruses are similar in several ways: both are negative strand, category IV RNA viruses; both infect cells of the immune system; both exit an infected cell by budding and spread through the body in circulating infected cells. If these viruses are so similar, why do they differ so dramatically in their symptoms and mortality (death) rates? To answer this question, you will need to know more about the ecology and biology of each virus. The ecology of a virus involves the interaction that a virus has with the host that serves as its environment and the mechanism by which a virus is transmitted from one host to another. The biology of a virus describes the structure of the virus; the mechanisms by which it enters a cell, makes copies of itself (reproduces), and exits the cell; and how it causes symptoms of disease in its host

II. The ecology of Ebola virus

Many viruses, especially those that cause emerging diseases, are able to infect and reproduce in more than one host species. In some cases, a host may not display disease symptoms (asymptomatic) despite the viral infection. This kind of host species is termed a reservoir host. However, when the virus is transmitted to a different species, it can cause a severe, often fatal, disease. The existence of reservoir hosts makes the eradication of certain kinds of viruses difficult, if not impossible.

Identification of the reservoir host of the Ebola virus has been elusive. Recent evidence has implicated bats as the source of infection but this remains to be proven as, to date, Ebola Virus has never been isolated from a bat. It is speculated that if bats are the reservoir, humans could become infected through contact with bat guano, from a bite, or through using bats as a food source. Once a human is infected, transmission from person to person occurs only by direct contact with blood and body fluids such as saliva, mucus, vomit, feces, sweat, tears, breast milk, urine, and semen.

III. The biology of Ebola virus

Ebola virus is made up of a single strand of RNA (negative strand) that is surrounded by proteins and a membrane, which form a long, filamentous structure (see Ebola virus in Table 3). The virus’ first line of attack is infection of cells that make up the immune system, the body’s major defense against infectious agents. The virus binds to the surface of the cell and is taken inside the cell where it releases its genetic material and enzymes needed for virus growth. Inside the cell, the virus makes many copies of itself through the following steps:

  1. Viral RNA polymerase transcribes mRNA from the negative-strand viral RNA.
  2. Using the host protein synthesis machinery, the mRNA directs the synthesis of viral structural proteins and enzymes.
  3. Viral RNA polymerase uses the negative-strand RNA also as a template for the production of a full-length positive-strand RNA as a step in the production of new virus particles (progeny).
  4. Viral RNA polymerase uses the positive-strand RNA (step 3) as a template for the production of full-length negative-strand RNA genomes.
  5. The negative-strand RNA genome, the viral RNA polymerase, and the structural proteins join together to form enormous numbers of viral particles.
  6. The virus exits the cell by budding from the host cell, picking up a coating of host membrane as it leaves.

Infection of the immune cells by Ebola virus causes havoc in many ways. It inactivates the very cells whose function it is to destroy a viral invader. Other functions of the immune system are activated inappropriately, causing the lining of blood vessels to leak blood and fluids, resulting in the internal bleeding in some Ebola patients. Large numbers of virus particles circulating in the blood can also infect liver cells, producing more particles, killing the liver cells, and leading to organ failure and characteristic symptoms of high fever, muscle aches, malaise, vomiting and diarrhea. Although no treatments were available for past outbreaks and epidemics, testing during the most recent Ebola outbreaks of a vaccine and antiviral drugs have shown promising results.

IV. The ecology of Measles virus

Measles virus is an example of a virus with no reservoir host. Humans are the only hosts. For this reason, the eradication of measles is possible, provided at least 95% of the population is immune, most reasonably through vaccination.

V. The biology of Measles virus

Measles virus shares many characteristics similar to Ebola virus. It is made up of a single strand of RNA (negative strand) that is surrounded by proteins and a membrane (see measles virus in Table 3). Unlike Ebola, which requires direct contact with body fluids, measles infection occurs when a person inhales virus-laden droplets exhaled from an infected person. The virus particles enter the lungs and, like Ebola, attack immune cells, the body’s first line of defense against infectious agents. The virus binds to the surface of the cell and is taken inside the cell where it releases its genetic material and enzymes needed for virus growth. Inside the cell, the virus makes many copies of itself through steps characteristic of negative-strand RNA viruses:

  1. Viral RNA polymerase transcribes mRNA from the negative-strand viral RNA.
  2. Using the host protein synthesis machinery, the mRNA directs the synthesis of viral structural proteins and enzymes.
  3. Viral RNA polymerase uses the negative-strand RNA also as a template for the production of a full-length positive-strand RNA as a step in the production of new virus particles (progeny).
  4. Viral RNA polymerase uses the positive-strand RNA (step 3) as a template for the production of full-length negative-strand RNA genomes.
  5. The negative-strand RNA genome, the viral RNA polymerase, and the structural proteins join together to form enormous numbers of viral particles.
  6. The virus exits the cell by budding from the host cell, picking up a coating of host membrane as it leaves.
  7. The infected cells, laden with viral particles, migrate from the lungs to the lymph nodes, infecting more immune cells and spreading the virus to other sites in the body, including the spleen, thymus, and skin. The skin rash characteristic of measles is the result of infection of cells in the skin. In some cases, the virus can reach the brain, where it may cause permanent brain damage.

    After several days, the viral-infected cells reach the nasal passages, infecting epithelial cells that line the upper respiratory tract and producing large numbers of viral particles. Infected individuals release clouds of virus-laden droplets from their noses, trachea, tonsils, and lungs. These droplets can remain infectious on surfaces for several hours and can move via air currents to the next susceptible host. This mode of transmission makes the measles virus highly contagious. Besides a rash, other symptoms of measles include coughing, runny nose, and red watery eyes that result from virus infection and cell death and a high fever, a sign of the immune system doing battle. In some instances, measles can lead to more serious symptoms and even death. Prior to the development of an effective vaccine in the early 1960s, 7 to 8 million children died of measles worldwide every year. By 2014 that number was reduced to 145,000.

    Because immune cells are a major site of virus reproduction, a bout of measles can leave the victim with an immune system that is somewhat disabled, making that person vulnerable to other infections. Recent studies have indicated that following an infection, a child’s immune system can be weakened for up to three years, leaving the child susceptible to infections that a fully functional immune system would normally fight off.

VI. Comparing Ebola Virus and Measles Virus
Ebola Measles
Similarities
Negative single-strand RNA Negative single-strand RNA
Infect cells of immune system Infect cells of immune system
Virus buds from cell Virus buds from cell
Spreads in body via infected cells Spreads in body via infected cells
No vector No vector
Incubation period 2–21 days Incubation period 7–14 days
Symptomatic transmission Symptomatic transmission
Likely immunity after infection Definite immunity after infection
Effective vaccine Effective vaccine
Differences
Not very contagious (R0 = 2) Extremely contagious (R0 = 18)
Infects dendritic cells and macrophages but not lymphocytes Infects dendritic cells and lymphocytes
Transmission – direct contact Transmission ‒ aerosol
Animal reservoir No animal reservoir
High fatality rate (50–90%) Moderate fatality rate (1–30%)