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Animal & human viruses
Viruses of humans and other animals. The Baltimore classification. HIV life cycle.
Key points:
- There are many different kinds of viruses that infect humans and other animals, some causing serious illness and others not.
- Viruses can be classified according to the Baltimore system, and human-infecting viruses fall into all of its seven categories.
- The human immunodeficiency virus (HIV), which causes acquired immune deficiency syndrome (AIDS), is a retrovirus.
Introduction
Have you ever had the flu or the chicken pox? If so, then you've had a close encounter of the viral kind! Whether you dream of one day finding a cure for AIDS or simply hope to avoid this year's flu bug, you're probably familiar with the suffering that can be caused by viral infections (and minimized by vaccines and treatments).
Human viruses come in many types and have a wide range of effects. Some make us sick for a day or two before going away, while others are lifelong. Some are a minor annoyance, while others, such as Ebola, can cause life-threatening complications.
Because of their impact on our health and quality of life, many human viruses (and related animal viruses) have been studied in detail. Let's take a look at some of these viruses.
What does an animal virus look like?
Like other viruses, animal viruses are tiny packages of protein and nucleic acid. They have a protein shell, or capsid, and genetic material made of DNA or RNA that's tucked inside the caspid. They may also feature an envelope, a sphere of membrane made of lipid.
Animal virus capsids come in many shapes. One of the craziest-looking (to me, at least) is the Ebola virus, which has a long, thread-like structure that loops back on itself. A more "standard-looking" virus, chikungunya, is shown below for comparison: chikungunya looks like a sphere, but is actually a
Animal virus genomes consist of either RNA or DNA, which may be single-stranded or double-stranded. Animal viruses may use a range of strategies (including some surprising and bizarre ones) to copy and use their genetic material, as we'll see in sections below.
How do animal viruses infect cells?
Animal viruses, like other viruses, depend on host cells to complete their life cycle. In order to reproduce, a virus must infect a host cell and reprogram it to make more virus particles.
The first key step in infection is recognition: an animal virus has special surface molecules that let it bind to receptors on the host cell membrane. Once attached to a host cell, animal viruses may enter in a variety of ways: by endocytosis, where the membrane folds in; by making channels in the host membrane (through which DNA or RNA can be injected); or, for enveloped viruses, by fusing with the membrane and releasing the capsid inside of the cell.
After the virus uses the host cell's resources to make new viral proteins and genetic material, viral particles assemble and prepare to exit the cell. Enveloped animal viruses may bud from the cell membrane as they form, taking a piece of the plasma membrane or internal membranes in the process. In contrast, non-enveloped virus particles, such as rhinoviruses, typically build up in infected cells until the cell bursts and/or dies and the particles are released.
Consequences of an infection
Viruses are associated with a variety of human diseases.
The diagram below shows some common examples of viral infections that affect different systems of the human body:
Some viral infections follow the classic pattern of acute disease: symptoms worsen for a short period, but in most cases, the virus is cleared from the body by the immune system and the patient recovers. Examples include the common cold and influenza.
Other viruses, such as the hepatitis C virus, cause long-term chronic infections. Still other viruses, such as human herpesviruses 6 and 7, which in some cases cause the minor childhood disease roseola, may form productive infections (ones where new viral particles are produced) without causing any symptoms at all in the host. In these cases, patients are said to have an asymptomatic infection.
Classifying animal viruses
Animal viruses come in many types, and they enter, commandeer, and exit cells in a variety of different ways. How can we organize this mess of viruses in a way that's consistent and makes sense?
The Baltimore system groups viruses according to their type of genetic material and how it's used to make messenger RNAs (mRNAs), key intermediates in the production of viral proteins and the assembly of new viruses. A virus's Baltimore group depends on:
- The molecule it uses as genetic material (DNA or RNA)
- Whether the genetic material is single- or double-stranded
- The steps the virus uses to make an mRNA
The Baltimore system divides viruses into seven groups. You can see the basic features of each group, including its genetic material and the pathway it uses to make an mRNA, in the diagram below:
Human viruses are found in all seven Baltimore groups, while plant and bacterial viruses are found only in a subset of groups.
The retrovirus HIV-1
Retroviruses, found in Baltimore group VI, have a unique and fascinating life cycle. They are of special importance because human immunodeficiency virus (HIV), the virus that causes acquired immune deficiency syndrome, or AIDS, is a retrovirus.
A retrovirus genome is single-stranded RNA and comes in two copies per viral particle. The RNA must be converted into double-stranded DNA by an enzyme called reverse transcriptase, reversing the normal flow of information from DNA to RNA to protein in cells.
The double-stranded DNA enters the nucleus of the host cell and is inserted into the host genome by an enzyme called integrase. mRNA can then be made by transcription of the viral DNA, which, as a permanent part of the host cell's genome, is called a provirus. The mRNA is read to produce viral proteins and may also serve as a genome for new viral particles that assemble and bud from the cell.
The diagram below shows the key life cycle stages of the HIV-1 virus, the strain responsible for most cases of HIV infection.
Anti-HIV drugs inhibit viral replication at many different phases of the HIV cycle. These drugs include:
- Fusion inhibitors, which block fusion of the HIV viral envelope with the plasma membrane of the host cell
- Reverse transcriptase inhibitors, which impair the conversion of the RNA genome into double-stranded DNA
- Integrase inhibitors, which inhibit the integration of the viral DNA into the host genome
- Protease inhibitors, which block processing of viral proteins
"Cocktails" containing multiple drugs are usually most effective at slowing the progression of the infection and keeping viral levels low. You can learn why this is the case in the virus evolution article.
For more on symptoms, treatment, and prevention of HIV and AIDS, please see the Health & Medicine section on HIV and AIDS.
Explore outside of Khan Academy
Do you want to learn more about the life cycle of HIV? Check out this scrollable interactive from LabXchange.
LabXchange is a free online science education platform created at Harvard’s Faculty of Arts and Sciences and supported by the Amgen Foundation.
Want to join the conversation?
Why would viruses ever use RNA(-) if all it does is provide extra work to turn it into RNA(+)?(5 votes)
Short answer: it works well enough to survive — note that some of the most pathogenic viruses are RNA(-).
Long answer (rampant speculation warning) — proposed advantages for RNA(-) viruses:
1) Allows the virus to make many mRNAs from a single infecting RNA(-) genome rather than being limited to transcription from a single RNA(+) genome, this is an extra step but it allows the virus to amplify its output of proteins and RNA as it takes over the cell
2) Increases viral efficiency by allowing the different viral genes to be expressed at different levels — genes near the 3' end get expressed at higher levels than those nearer the 5' end (see refs for details).
3) Since they carry their own replication machinery these viruses aren't as dependent on host factors and so may be able to infect a broader range of hosts — this also means they have more freedom to evolve.
You can read more about these hypotheses on the following pages:
http://www.bio.net/hypermail/virology/1994-October/000905.html
https://www.reddit.com/r/askscience/comments/2zu5eg/is_there_any_benefit_of_an_rna_virus_being/
https://www.quora.com/Do-negative-sense-RNA-viruses-have-an-advantage-over-positive-sense-RNA-viruses(6 votes)
Where do prions fit in the virus/bacteria/etc. classification? For example the prion that causes Creutzfeldt–Jakob disease?(2 votes)
Prions are an entirely separate class of disease from viruses, bacteria, fungus, and protists. When proteins are created, they are originally just a chain of amino acids which are then folded into a specific 3-dimensional shape. The primary theory at this point is that a prion is a mis-folded protein. When the prion comes into contact with a protein that is chemically but not structurally identical to itself, it causes the other protein to spontaneously re-fold into the shape of the prion. When the protein re-folds it becomes unusable for the cell. When this occurs enough times, the cell is unable to function properly and dies, releasing the prions to contact other cells where the process is repeated until the organism dies (usually from extensive brain damage). If you need further information I would recommend reading the book "Deadly Feasts" by Richard Rhodes.(5 votes)
How does the viral genetic code know what to do once inside a cell?(2 votes)
The viral genome is actually much like a cookbook which contains all the instructions whereas the enzymes and proteins are the chefs that do the work.(4 votes)
what the difference between eukaryocytes and prokaryocytes?(1 vote)- 1) Eukaryotes have a membrane-bound nucleus in which they store their genetic material, while prokaryotes do not. Prokaryotes store their genetic material in a cluster in the cytoplasm called a nucleoid.
2) Eukaryotic cells are much bigger than prokaryotic cells. For comparison, most prokaryotes are 0.2 - 2 μm (1 μm = 0.001 millimetres), whilst eukaryotes are generally 10 - 100 μm.
3) Lastly, prokaryotic cells lack organelles. For example, prokaryotes do not contain mitochondria or chloroplasts. Their ribosomes (organelles used for protein synthesis) are smaller than those of the eukaryote.
There are many more differences, however these are the most notable. To help understand the topic better, you could look at Khan Academy's "Bacteria and Archaea" section.(4 votes)
Does (-) sense RNA have to first transcribe into (+) RNA to then transcribed back to (-) RNA? I'm confused as to why (-) sense RNA has RNA dependent RNA polymerase. Also what determines whether a (+) sense RNA strand will be transcribed into a (-) sense RNA or reverse-transcribed to DNA (as in retroviruses).(2 votes)- Ss-Rna can be of negative polarity or positive polarity. In case of positive sense Rna...It acts a template for the production of more rnas alike and also as mrna to translate capsomeres that together form the capsid,tegumental proteins and other enzymes and proteins aiding in the process.
The negative sense ss Rna is not capable of causing infection .Henceforth it is replicated into positive strand ss Rna which then acts as a template to replicate more negative ss Rna(that of its progenies) as well as positive ss Rna to translate them into capsomeres which constitute the capsid , tegumental protein and various enzymes and proteins that aid in the process.
Now retroviruses,exhibit a unique replicative cycle.The ss Rna is converted into a Rna:dna hybrid by the viral enzyme (reverse transcriptase) and then a Double stranded dna is synthesized from this hybrid called the provirus which is then injected into the host cell..Which then acts as a template for the synthesis of its progeny Rna.And the genetic code of different viruses is the determining factor
for which way it would be replicated, transcribed or translated.
Hope this helps!(1 vote)
- Herpes virus synthesizes its lipoprotein envelope with its host nuclear membrane's aid but why does it not incorporate itself within the host cell plasma membrane , once eluding from the cell?
So what is it that drives the synthesis of a lipoprotein envelope? Is it correlated to the polarity of the outermost covering of a virus? Or in case of glycoproteins something even more fascinating?(2 votes)
That is an interesting question.
Probably it is more effective to leave the host cell, not to integrate into the cell membrane of the host.
Glycoproteins are those who drive lipoprotein synthesis and integration, look at this paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373811/(1 vote)
If a cat gets a disease and passes it onto a human can the human then pass this same disease to a dog?(2 votes)- It really depends on virus.
However, animal viruses are not that flexible and compatible among different species such as cat -> human -> dog.
I can think of the Influenza virus which is possibly transmissible from ducks to pigs than to humans H1N1, but in the meantime, receptors evolve in pig lungs before they reach humans.(1 vote)
'To turn its host cell into a "virus factory," the virus must induce the cell to make viral proteins, and the only way to do that is by providing an mRNA for the cell's translation machinery to read.'
I couldn't understand this part. Please help. Thank you.(1 vote)- Some viruses have an RNA genome and before integrating their genome into that of a host cell, it must use the enzyme reverse-transcriptase to create DNA. I hope this helps :)(2 votes)
Where does viruses steal the DNA or RNA?(1 vote)- They do nto steal, they usually steal host reproductive machinery.
They can steal chunks of genetic material from previous hosts I suppose and then evolve.(1 vote)
- What do all viruses have in common concerning their in vitro cultivation?(1 vote)
- The fact that they are intracellular parasites.
They have nucleic acid (DNA or RNA) never both and they have capsid - protein structure.(1 vote)