IV. VIRUSES

C. VIRAL STRUCTURE

The overall purpose of this Learning Object is to learn the chemical makeup and the various structural components of which viruses are made.

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


A. Viral Structure

Since viruses are not cells, they are structurally much more simple than bacteria. An intact infectious viral particle is called a virion (def) and consists of:

1. A genome (def)

The viral genome is a single or segmented, circular or linear molecule of nucleic acid functioning as the genetic material of the virus. It can be single-stranded or double-stranded DNA or RNA (but never both), and codes for the synthesis of viral components and viral enzymes for replication.

2. A capsid

The capsid (def), or core, is a protein shell surrounding the genome and is usually composed of protein subunits called capsomeres (def). The capsid serves to protect and introduce the genome into host cells. Some viruses consist of no more than a genome surrounded by a capsid and are called nucleocapsid or naked viruses (def) (see Fig. 2A and Fig. 2B). Attachment proteins project out from the capsid and bind the virus to susceptible host cells.

3. An envelope

Most animal viruses also have an envelope surrounding a polyhedral or helical nucleocapsid, in which case they are called enveloped viruses (see Fig. 2C, Fig. 2D,and Fig. 3). The envelope is composed of phospholipids and glycoprotein and for most viruses, is derived from host cell membranes by a process called budding (see Fig. 4 and Fig. 3B). The envelope may come from the host cell's nuclear membrane, vacuolar membranes (packaged by the Golgi apparatus), or outer cytoplasmic membrane.

Although the envelope is usually of host cell origin, the virus does incorporate proteins of its own, often appearing as glycoprotein (def) spikes, into the envelope. These glycoprotein spikes function in attaching the virus to receptors on susceptible host cells.

B. Viral Activation of Innate Immunity

In order to protect against infection, one of the things the body must initially do is detect the presence of microorganisms. The body does this by recognizing molecules unique to microorganisms that are not associated with human cells. These unique molecules are called pathogen-associated molecular patterns or PAMPs (def). (Because all microbes, not just pathogenic microbes, possess PAMPs, pathogen-associated molecular patterns are sometimes referred to as microbe-associated molecular patterns or MAMPs.)

For example, most viral genomes contain a high frequency of unmethylated cytosine-guanine dinucleotide sequences (a cytosine lacking a methyl or CH3 group and located adjacent to a guanine). Mammalian DNA has a low frequency of cytosine-guanine dinucleotides and most are methylated. In addition, most viruses produce unique double-stranded viral RNA, and some viruses produce uracil-rich single-stranded viral RNA during portions of their life cycle. These forms of viral nucleic acids are common PAMPs associated with viruses. These PAMPs bind to pattern-recognition receptors or PRRs (def) called toll-like receptors or TLRs found within the endosomes of phagocytic cells. Viral RNA can also bind to cytoplasmic PRRs called RIG-1 (retinoic acid-inducible gene-1)and MDR-5 (melanoma differentiation-associated gene-5).

Most of the PRRs that bind to viral components trigger the synthesis of cytokines (def) called Type-I interferons (def) that block viral replication within infected host cells. The TLRs for viral components are found in the membranes of the phagosomes used to degrade viruses during phagocytosis. As viruses are engulfed by phagocytes, the viral PAMPS bind to TLRs located within the phagolysosomes (def) (endosomes (def)). The TLRs for viral components include:

1. TLR-3 binds double-stranded viral RNA;
2. TLR-7 binds uracil-rich single-stranded viral RNA such as in HIV;
3. TLR-8 binds single-stranded viral RNA;
4. TLR-9 binds unmethylated cytosine-guanine dinucleotide sequences (CpG DNA) found in bacterial and viral genomes.

5. RIG-1 (retinoic acid-inducible gene-1) and MDA-5 (melanoma differentiation-associated gene-5), are cytoplasmic sensors that both viral double-stranded and single-stranded RNA molecules produced in viral-infected cells

 

Viral components also activate the alternative complement pathway and the lectin pathway, defense pathways that play a variety of roles in body defense.

To view electron micrographs of a variety of viruses, Linda Stannard's web page at the University of Capetown. Also see the web page at Queens University at Belfast.

Bacteriophages are viruses that only infect bacteria. Some bacteriophages are structurally much more complex than typical nucleocapsid or enveloped viruses and may possess a unique tail structure composed of a base plate, tail fibers, and a contractile sheath (also see Fig. 1C and Fig. 2E). Other bacteriophages, however, are simple icosahedrals or helical (see Fig. 1C).

 

     

     

 

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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