IV. VIRUSES

F. ANIMAL VIRUS LIFE CYCLES

2. The Productive Life Cycle with Possible Latency

The overall purpose of this Learning Object is to learn how some animal viruses can become latent within their hosts.

LEARNING OBJECTIVES FOR THIS SECTION

Viruses are infectious agents with both living and nonliving characteristics.

1. Living characteristics of viruses

a. They reproduce at a fantastic rate, but only in living host cells.

b. They can mutate.

2. Nonliving characteristics of viruses

a. They are acellular, that is, they contain no cytoplasm or cellular organelles.

b. They carry out no metabolism on their own and must replicate using the host cell's metabolic machinery. In other words, viruses don't grow and divide. Instead, new viral components are synthesized and assembled within the infected host cell.

c. TThe vast majority of viruses possess either DNA or RNA but not both.

Latent Life Cycle of Animal Viruses (Productive Life Cycle with Possible Latency)

Some double-stranded DNA animal viruses such as the herpes viruses, and a group of viruses known as the retroviruses (def) are able to remain latent (def) within infected host cells for long periods of time without replicating or causing harm. Some of these viruses remain latent within the cytoplasm of the host cell while others are able to insert or integrate their DNA into the host cell's chromosomes. When the viral DNA is incorporated into the host cell's DNA, it is called a provirus (def).

Viral latency is thought to result primarily from the lack of production of specific host cell proteins that are required for the activation of the viral genes responsible for turning on viral replication. As long as these specific host cell proteins are not being made by the host cell, the virus can't replicate. However, because the virus is inside the infected cell, it also can't be removed by the body's immune responses and the person may carry the virus throughout their life.

Subsequent activation of the host cell's DNA in response to extracellular stimuli, however, can lead to synthesis of the specific host cell proteins required by the virus and these proteins now activate the viral genes leading to a burst of viral replication via the productive life cycle (def).

Herpes viruses, for example, are often latent in some cell types but productive in others. Herpes viruses include herpes simplex type 1 (HSV-1) which usually causes fever blisters or oral herpes, herpes simplex type 2 (HSV-2) which usually causes genital herpes, Epstein-Barr virus (EBV) which causes infectious mononucleosis and plays a role in certain cancers, varicella-zoster virus (VZV) which causes chickenpox and shingles, and cytomegalovirus (CMV) which causes a variety of infections in immunosuppressed persons and is also a leading cause of birth defects. (For more on HSV and CMV, see the AIDS Pathology Tutorial at the University of Utah.)

In the case of HSV-1, HSV-2, and VZV, primary infection causes the virus to replicate within epithelial cells (def). However, some of the viruses enter and migrate down neurons (def) where they become latent in the body of sensory neurons. Subsequent activation of the latently infected neurons by a variety of extracellular stimuli enables the viruses to migrate back up the nerve cell and replicate again in the epithelial cells.

- Scanning electron micrograph of HSV; courtesy of Dennis Kunkel's Microscopy.

With EBV, the virus is productive in epithelial cells but latent in B-lymphocytes (def).

     

 


In the case of HIV, the viral genome eventually becomes a provirus (def). After integration, the HIV proviral DNA can exist in either a latent or productive state, which is determined by genetic factors of the viral strain, the type of cell infected, and the production of specific host cell proteins.

The majority of the proviral DNA is integrated into the chromosomes of activated T4-lymphocytes. These generally comprise between 93% and 95% of infected cells and are productively infected, not latently infected. However, a small percentage of HIV-infected memory T4-lymphocytes persists in a resting state because of a latent provirus. Subsequent activation of the host cell by extracellular stimuli, however, causes the needed proteins to be made and the virus again replicates via the productive life cycle.These memory T4-lymphocytes, along with infected monocytes, macrophages, and dendritic cells, provide stable reservoirs of HIV capable of escaping host defenses and antiretroviral chemotherapy.

In the next section we will now look at the life cycle of HIV.

 

E-Medicine article on infections associated with organisms mentioned in this Learning Object. Registration to access this website is free.

 

Student-Authored Descriptions of Viral Infections

Astroviruses by Michele Stedding

Coxsackievirus by Mandy Hughes

Coxsackievirus by Salyna Riggs

Cytomegalovirus (CMV) by Cindi Chou

Ebola by Christine Sprinkle

Ebola by Dianne Bettick

Ebola by LaTanya Gary

Epstein-Barr Virus (EBV) by Erica Rome

Hantavirus by Jennifer Robinson

Hepatitis A (HAV) by Anastasiya Lyudkevich

Hepatitis B (HBV) by Karen Neff

Hepatitis C (HCV) by Rosemary Bewley

Hepatitis C (HCV) by Corinne Borel

Herpes Simplex types 1 and 2 (HSV1 &HSV2) by Katrina Armstrong

Herpes Simplex types 1 and 2 (HSV1 & HSV2) by Cindy Dubs

Herpes Simplex type 2 ( HSV2) by Lauren Bentley

Human Immunodeficiency Virus (HIV) by Steven Merrill

Human Papilloma Viruses (HPV) by Megan Johnson

Human Papilloma Virus (HPV) by Laura Moy

Influenza by Kenneth Agboifo

Measles (Rubeola) by Peggy Engel

Measles (Rubeola) by Sumara Choudhry

Measles (Rubeola) by Yashu Karki

Mumps by Trudy Ann Hinds

Noroviruses by Kristina Garner

Poliomyelitis by Deborah Malin

Rabies by Pamela Russillo

Rabies by Lauren Mekalian

Rhinoviruses (colds) by Nina Mezu

Rift Valley Fever by LaWanda Morgan

Respiratory Syncytial Virus (RSV) by Ben Kaufman

Respiratory Syncytial Virus (RSV) by Christen Strickler

Rotaviruses by Chrissy Blake

Rotaviruses by Shana Lucas

Varicella (chickenpox) by Rosemary Brunet

Varicella (chickenpox) by Violeta Genova

Viral Meningitis by Denise Grandea

 

 

 

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