Module 4: Viruses

CommentaryTopicsViral CharacteristicsViral TaxonomyViral StructureViral Nucleic AcidAnimal Virus Life CycleFate of Viral InfectionsHuman Immunodeficiency Virus (HIV)Vaccines and VirusesViruses and CancerPrionsOverview of Viruses that Affect HumansConclusion

Viral CharacteristicsViruses are obligate intracellular parasites, which means that they cannot multiply outside of a host cell. They can survive for a short while on surfaces, which enables them to pass from person to person. For example, when an individual infected with a respiratory virus sneezes, he or she expels tiny droplets of moisture containing the virus. These droplets can persist on surfaces (such as a keyboard or a restaurant table), waiting to be picked up by another host, for hours or even days, depending on the surface and the type of virus.

Viruses are acellular, which means that they are not composed of cells. They do not contain cytoplasm or organelles, and they cannot replicate their genomes. Viruses are made up of proteins and genetic material in the form of either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA). We will take a closer look at the genetic makeup of viruses later in this module.

Viruses have a specific host range, which means that they can only infect certain host species and cell types. For example, human T-cell leukemia virus (HTLV) causes leukemia in humans, but not in other animals. Similarly, feline leukemia virus (FeLV) causes leukemia in cats, but not in humans or other animals. Although these two viruses are similar and result in similar diseases, they each have their own distinct host range.

Viruses belong to one of three groups, depending on their host range:

1. animal viruses2. plant viruses3. bacterial viruses

In this module, we will examine the structure and role of animal viruses—specifically, those that infect humans.

Viral TaxonomyViral taxonomy gives us a way to identify viruses based on their structural characteristics. Viruses have five categories of classification, as shown in figure 4.1:

Figure 4.1Viral Taxonomy

Each category has its own suffix (ending). For example, if a viral name ends in "-virales," this indicates that it is of a viral order, and if it ends in "-viridae," this indicates that it is of a viral family.

Like bacteria, viruses have a nomenclature scheme. In module 3, we learned about the binomial nomenclature used to indicate bacterial genus and species. Viral nomenclature uses the common name in place of the formal Latinized genus and species names.

For an example, let's look at the naming scheme of the virus that causes herpes in humans:

Family name: Herpesviridae Genus: Simplexvirus Common name: Herpes simplex virus (refers to type 1 or 2)

In this course, you will most often encounter the family and common names of viruses.

Viral StructureViruses are among the smallest microbes known to cause disease. In module 1, we learned that the Escherichia coli bacterium is approximately 2 micrometers (μm), or 2,000 nanometers (nm), in length, which is equal to about one-five hundredth the thickness of a dime. Viral particles are considerably smaller than most bacterial cells. For example, the

smallpox virus (one of the largest) is about 0.25 μm (or 250 nm) in length, and one of the viruses causing the common cold has a length of about 0.07 μm (or 70 nm). The small size of viruses delayed their discovery until the 1900s, when microscopes became powerful enough to visualize the tiny particles. Prior to this, scientists suspected the existence of viruses, but could not prove it.

A single viral particle is known as a virion. Each virion consists of the following parts:

nucleic acid (viral genome): genetic material that takes the form of either DNA or RNA, depending on the virus

capsid: protective protein coat surrounding the nucleic acid viral proteins: various proteins, including enzymes the virus uses while in the host

cell envelope: phospholipid membrane surrounding the capsid; not all viruses have this

Figure 4.2 shows these components:

Figure 4.2Components of a Typical Virion

The viral envelope is similar in structure to the plasma membrane of a cell. The virus actually acquires the envelope by "stealing" part of the host cell membrane as it leaves the cell. We will examine this process later in this module.

Envelopes often contain viral proteins called spikes that project from the envelope and help the virus attach to and infect the host cell. Some viruses, such as the influenza virus, have spikes that change or mutate over time, which is why the flu vaccine (which targets the spikes) is only effective for one season. The influenza virus that comes around next year will have a different set of viral spikes than the one that came around this year, rendering this year's vaccine ineffective.

Viruses come in three shapes, based on their capsid structure:

1. icosahedral viruses resemble a twenty-sided ball2. helical viruses resemble a spring3. complex viruses come in a variety of shapes

Figure 4.3 shows examples of enveloped and non-enveloped icosahedral, helical, and complex viruses:

Figure 4.3Viral Structures

Sources: CDC, 1981, CDC Web site; Jones, 2006, Wikipedia Web site; USDA, USDA Web site; Williams, 2007,EPA Web site; Wikipedia, 2007, Wikipedia Web site; Wikipedia, 2008, Wikipedia Web site. Some ofthese images are in the public domain and some are used with permission under the terms of the

GNU Free Documentation License and the Creative Commons Attribution Sharealike License.

Viral Nucleic AcidViral genomes are composed of either DNA or RNA, depending on the virus. They can be double-stranded (ds), similar in structure to the cellular DNA ladder, or they can be single-stranded (ss), similar in structure to cellular RNA.

Single-stranded viral genomes are labeled (+) or (–) depending on their orientation, or the direction of their nucleotides. Cellular DNA is antiparallel, which means that the two DNA strands are orientated opposite each other like two lanes of opposing traffic. The strand with the nucleotides assembled from left to right is the (+) strand, and the strand with the nucleotides assembled from right to left is the (–) strand.

Figure 4.4 illustrates the different orientations of viral nucleic acids:

Figure 4.4Orientation of Viral Genomes

There are seven viral genome groups, distinguished by the structure of their nucleic acid. Table 4.1 compares these groups:

Table 4.1Viral Genome Groups

Group DNA or

RNA

Nucleic Acid Type and

Orientation

Examples of Viruses

Examples of Disease(s) Caused

I DNA double-stranded adenoviruses respiratory illnesses

II DNA (+) single- parvoviruses fifth disease

Group DNA or

RNA

Nucleic Acid Type and

Orientation

Examples of Viruses

Examples of Disease(s) Caused

stranded (childhood rash)

III RNA double-stranded reoviruses gastroenteritis

IV RNA (+) single-stranded

picornaviruses polio, foot and mouth disease, common cold, hepatitis A (HAV)

V RNA (–) single-stranded

orthomyxoviruses influenza

VI RNA single-stranded retroviral

HIV AIDS

VII RNA double-stranded retroviral

hepadnaviruses hepatitis B (HBV)

In module 2, we learned how a cell enacts transcription and translation to convert genetic information into usable proteins. Transcription is the process of copying genetic information from DNA nucleotides into RNA nucleotides, and translation is the process of building proteins out of amino acids using the information contained in the RNA nucleotide sequence.

Viruses carry very few proteins and enzymes with them in their capsid. They lack most of the proteins necessary to accomplish transcription, translation, and even replication. To compensate for this, they use host cell machinery, manipulating it for their own purposes to convert their genetic information into the proteins they need in order to multiply and create new virions.

Figure 4.5 shows the process of creating proteins as accomplished by each genome group:

Figure 4.5Viral Genome Translation in Host Cell

As you can see, single- and double-stranded RNA retroviruses use the viral enzyme reverse transcriptase to convert viral RNA into DNA. This DNA becomes a permanent part of the host cell's DNA and is transcribed and translated by the host cell for the rest of the host's life.

Animal Virus Life CycleAs viruses are intracellular parasites, their life cycle requires the presence of a host cell. For animal viruses, the host cell is an animal cell. Other viruses, such as plant and bacteria viruses, use non-animal cells to complete their life cycle. In this module, we will study the life cycle of a typical animal virus.

The animal virus life cycle has five stages:

1. attachment2. entry3. uncoating4. biosynthesis5. maturation and release

We will examine each of these in detail in the following sections.

Attachment

In module 3, we learned that some bacteria can cause disease without attaching to a host cell, such as by secreting toxins. In contrast, viruses must attach to a cell to produce an infection. Viral particles attach to specific host cell receptor proteins located on the surface of the host cell.

The attachment site of a virus varies depending on the viral type. For example, the influenza virus uses the spikes on its envelope to bind to host cell receptors. Adenoviruses, which cause respiratory infections and conjunctivitis, attach to host cells using small fibers on their icosahedral capsid. Figure 4.6 shows an influenza virus attaching to a host cell:

Figure 4.6Influenza Viral Attachment

Host cell receptor proteins are inherited, which means that you have the same receptors on your cells as your parents have on theirs. Receptor proteins perform various functions in the body, such as sensing chemical and hormonal signals and gathering nutrients for cells.

Viruses hijack these receptor proteins when they bind to host cells. Each type of virus binds to a specific type of receptor. Whereas some receptors are universal or nearly so in a population, others may exist only in a subset. Your possession or lack thereof of a particular receptor determines your susceptibility to a particular virus. For example, if your cells lack the receptor used by the parvovirus, you cannot be infected with this virus, and are immune to fifth's disease.

Entry

Viruses enter the cell in one of two ways, depending on whether or not they have an envelope.

Enveloped viruses fuse with the host cell membrane. The viral envelope is very similar to the host cell membrane, and the virus can graft onto the membrane, dumping its contents into the host cell cytoplasm.

Non-enveloped viruses induce pinocytosis in the host cell. Pinocytosis is a natural cell process in which the plasma membrane pinches inward to bring extracellular material and nutrients into the cell.

Uncoating

Uncoating is the process by which the viral capsid separates from the viral nucleic acid. Once inside the host cell, the virus no longer needs its capsid, and sloughs it off to be digested by viral or host enzymes, depending on the virus type.

Figure 4.7 illustrates the processes of viral entry and uncoating for enveloped and non-enveloped viruses:

Figure 4.7Viral Entry and Uncoating

Biosynthesis

In a virus, biosynthesis is the process by which DNA or RNA is replicated for the purpose of making new viral particles (viral multiplication). Figure 4.8 shows how biosynthesis occurs for the viruses in each genome group. Biosynthesis relies on either viral or host enzymes, depending on the virus type.

Figure 4.8Viral Biosynthesis

In addition to the viral genome, viral and capsid proteins must be made for each new viral particle produced. A single virion that enters and infects a host cell is capable of producing hundreds or even thousands of new viral particles.

Maturation and Release

A mature virion contains a genome (DNA or RNA), a capsid, and various viral proteins and enzymes. Viral protein production, capsid formation, and virion assembly all occur in the host cell cytoplasm. Virion assembly is the packaging of viral proteins and the viral genome into the capsid in preparation for the viral particle's release from the host cell.

Enveloped viruses gain their envelope upon their release from the host cell in a process called budding. During budding, the virion pinches away from the cell, taking part of the

host cell plasma membrane with it. This can kill the cell, but it often does not. The virion inserts certain viral proteins into the stolen plasma membrane, and it becomes the viral envelope.

Non-enveloped viruses leave the host cell by rupturing the host cell plasma membrane, causing lysis. This process is highly destructive, and results in death of the host cell. Figure 4.9 illustrates the maturation and release process for both enveloped and non-enveloped viruses.

Figure 4.9Viral Maturation and Release

Fate of Viral InfectionsNot all viruses act in the same manner once they have established an infection inside a host. The path of a viral infection is largely determined by the viral type, and may be influenced by the host as well. Most viruses take one of three paths:

1. acute viral infection2. chronic viral infection3. latent viral infection

Acute viral infections involve the rapid production of new viral particles that can spread to neighboring cells and even to a new host through the environment (such as in a sneeze). These types of viral infections, such as the common cold caused by the rhinovirus, tend to result in the destruction of host cells and in overt symptoms of illness in the host. Acute viral

infections come from both enveloped and non-enveloped viruses. Symptoms such as runny nose, sneezing, coughing, and diarrhea promote the rapid spread of the disease to new hosts. Acute viral infections tend to last a few days to a few weeks.

Chronic viral infections, such as HIV and hepatitis B (HBV), have a longer course of action and can last for months, years, or even a lifetime. During this time, viral particles are made and released from the host cell at a much slower pace than in acute viral infections. Chronic viral infections are typically caused by enveloped viruses, which can exit the host cell continually over a long period of time without killing the cell.

Latent viral infections come from viruses that have a slow course of infection that results in long asymptomatic periods. These viruses can remain in the host cell for long periods of time without multiplying or causing harm. Some latent viruses stay in the cytoplasm, whereas others integrate permanently into the host cell's DNA. Some chronic viral infections, such as HIV and HBV, are considered latent viral infections depending on their state of activity (multiplication) or inactivity (non-multiplication) in the host.

Table 4.2 lists some viruses that cause latent infections:

Table 4.2Examples of Viruses that Cause Latent Infections

Virus Disease or Condition Caused

Herpes simplex virus 1 (HSV-1)

cold sores (fever blisters)

Herpes simplex virus 2 (HSV-2)

genital blisters

Varicella-zoster virus (VZV)

chicken pox (child) and shingles (adult)

Epstein-Barr virus (EBV) mononucleosis

Human immunodeficiency virus (HIV)

acquired immunodeficiency syndrome (AIDS)

Herpes simplex viruses, for example, remain in the host cells for the lifetime of the host. They lie dormant until reactivated with a stimulus. HSV-1, which causes fever blisters (cold sores), is reactivated through ultraviolet (UV) sun exposure and stress. Immunosuppression can also cause the reactivation of latent viruses. For example, the varicella-zoster virus (VZV), which causes chicken pox in children, remains latent in a person's nervous system. This virus may reactivate when people age or if they become immunosuppressed, causing shingles, a more dangerous, adult form of chicken pox.

Human Immunodeficiency Virus (HIV)The human immunodeficiency virus (HIV), the virus that causes AIDS, was first recognized in the early 1980s as a sexually transmitted viral illness. At first, HIV was

believed to be an illness of the male homosexual community. We now appreciate that the HIV epidemic is a worldwide phenomenon with no racial or sexual boundaries. In 2007, 33.2 million people worldwide lived with HIV. During 2007, 2.1 million people died of AIDS, and 2.5 million people became newly infected with HIV (WHO, 2007, WHO Web site).

HIV is a lentivirus (genus) from the Retroviridae family. Lentiviruses are characterized by slow growth and a long incubation period. A healthy individual can harbor HIV for years or even decades before the symptoms become noticeable. HIV is an enveloped, single-stranded (+) RNA retrovirus that, once inside the host cell, converts its viral RNA into DNA and integrates permanently into the host's DNA. Once part of the host's genome, HIV is protected from the immune system and cannot be eliminated without the death of the host cell.

Life Cycle of HIV

HIV binds to and infects T helper (also called Th or CD4+) immune cells. These cells display a CD4 receptor along with other receptors that HIV needs for attachment and entry. CD4+ immune cells circulate throughout the body, and are thus easily accessible to HIV. The major routes of infection for HIV are sexual intercourse and blood product and mother-child transmission (occurring prenatally or during birth). HIV becomes severely damaged when bodily fluids dry out, and therefore does not survive for long outside the host.

Figure 4.10 illustrates the life cycle of HIV, beginning with the infection of the CD4+ cell:

Figure 4.10HIV Life Cycle

Based on image from Beyer 2004, Wikipedia Web site

During the initial acute phase of HIV infection, the virus destroys large numbers of CD4+ cells, causing a weakening in the immune system. After the acute phase passes, HIV becomes a chronic infection, where the virus actually stimulates the immune system to increase CD4+ activity so that more viral particles can be created. The constant activation of the immune system, along with rise in HIV particles, eventually damages the host's CD4+ cells. This phase of the disease can last for years or decades without the production of overt symptoms in the infected individual.

HIV infection eventually leads to acquired immunodeficiency syndrome (AIDS), a condition in which the immune system is too severely damaged to protect the infected individual. With the disarming of the immune system, HIV opens the door to secondary infections such yeast infections caused by the fungus Candida or pneumonia caused by the bacterium Pneumocystis carinii.

Treatment of HIV

The progression of HIV/AIDS can be slowed with the use of antiretroviral medicines. Current treatment of HIV involves highly active antiretroviral therapy (HAART), a combination of several antiretroviral drugs. HIV is difficult to treat, as it is permanently integrated into the host's genome; the goal of antiretroviral drug therapy is to prevent the activation and growth of the latent virus in the CD4+ cells.

A good antiretroviral drug should

work against both normal and mutated forms of the virus prevent viral breakthrough (when the virus escapes the drug's effects unharmed) remain active in the patient for long periods of time (reducing the number of doses

needed) have minimal side effects be easy to produce (keeping costs down for companies and patients)

Vaccines and VirusesVaccines prevent disease by priming the immune system in anticipation of an attack. They show your immune cells a harmless piece of a specific pathogen. This initial exposure induces your immune cells to stockpile ammunition in case of attack from that pathogen. This ammunition takes the form of antibodies that roam around your body on a search-and-destroy mission. Antibodies are highly specific, and work only against the targeted pathogen. We will examine the process of antibody production and function in module 5.

Edward Jenner created the first effective vaccine in the late 1700s, curbing the spread of smallpox before anyone even knew its cause. The vaccine contained the closely related cowpox virus, which acted as a mechanism to stimulate the immune system to make antibodies against cowpox. These antibodies were similar enough to the smallpox variety to cross-react with the smallpox virus, destroying it before it could cause disease. Jenner's vaccine was so effective that, in 1980, the World Health Organization (WHO) declared smallpox officially eradicated.

The influenza vaccine targets the protein spikes on the viral envelope. These spikes are a natural target because of their exposed position on the virus. Influenza viral spikes vary from season to season, which is why we need a new vaccine each year. The vaccine contains only a few portions of the virus, and cannot actually give you the flu.

To create the influenza vaccine, scientists first determine which strain of the virus seems to be making its way across the globe. If they choose the correct strain, and few mutations occur between the time of vaccine production and the time of administration, the vaccine will be successful. Occasionally, scientists choose the wrong strain or a highly mutating strain. In these cases, the vaccine is either reduced in its effectiveness or completely ineffective. Ideally, you would get the influenza vaccine a few weeks to a month in advance of exposure to the virus to give your immune system the time it needs to create an army of antibodies.

The measles-mumps-rubella (MMR) vaccine is given in childhood to prevent three potentially severe diseases. This vaccine combines three live, attenuated (weakened) viruses. Although too frail to cause illness, attenuated viruses are hardy enough to prime the immune system and to induce antibody production. The limited mutation ability of these

viruses makes the vaccine highly effective, and it only needs to be given twice to induce long-term immunity.

Unfortunately, scientists have not yet found a way to create vaccines for all viral illnesses. One major challenge in HIV vaccine development is to create a substance that will not be rendered ineffective by the high mutation rate of HIV. Like influenza, HIV has the ability to alter the protein spikes protruding from its viral envelope. HIV can change its spikes more quickly than the immune system can make new antibodies. The changes may not be drastic—the replacement of a single amino acid in the protein spike can render an antibody ineffective. In order to create an effective HIV vaccine, researchers must find a target on the virus that will not mutate during an infection or when passed to another person.

Viruses and CancerA few viruses are known to cause cancer, although most cancers are not caused by viruses. In 1908, scientists first discovered a link between viral infection and cancer, finding that a virus causes chicken leukemia. The first oncogenic, or carcinogenic, human virus was not discovered until the 1970s.

The link between a viral infection and cancer can be difficult to detect. Not all people infected with the same virus develop cancer, and the cancer may manifest itself years after the initial infection. Additionally, whereas a virus is transmissible from person to person, cancer is not.

Viral cancers result when a virus changes the genetic composition of a cell, stimulating unregulated cell development cycles. Specifically, the virus turns on regions of the host genome known as oncogenes. Once activated, these regions cause uncontrolled cell growth, tumor formation, and cell and tissue destruction in the host. For this reason, cancer-causing viruses are known as oncogenic viruses. Host oncogenes can also be turned on (and made to cause cancer) through non-viral means, such as through exposure to chemicals and radiation.

Table 4.3 lists a few of the viruses known to cause cancer in humans:

Table 4.3Examples of Oncogenic Viruses

Virus Genome Type

Type of Cancer Caused

Human papillomavirus (HPV)

DNA cervical cancer

Epstein-Barr virus (EBV)

DNA Burkitt lymphoma

Hepatitis B (HBV) DNA liver cancer

Human T-cell leukemia virus (HTLV)

RNA leukemia

Hepatitis C (HCV) RNA liver cancer

PrionsPrions are a special group of infectious agents that do not fit well into either the bacterial or viral categories. However, as prions lack a classic cell structure, they are generally classified with viruses.

Prions are infectious proteins that lack nucleic acids, membranes, capsids, and envelopes.

Currently, we know of nine prion diseases that affect humans and animals. All are neurological diseases, including bovine spongiform encephalopathy (BSE, or mad cow disease), Creutzfeldt-Jakob disease (CJD), kuru, and the very rare fatal familial insomnia (FFI). All of these diseases are spongiform encephalopathies, which cause large vacuoles to develop in the brain.

Prions cause disease by altering the structure of a specific host cell protein called PrPc. Once altered, PrPc becomes PrPsc. This misshapen form of the protein can act as an infectious prion and alter even more host PrPc proteins. These alterations are permanent and eventually lead to degenerative tissue damage in the brain of the patient. Figure 4.11 summarizes the process by which a prion alters a host cell:

Figure 4.11Prion Infection of Host Cell

Prion diseases can be inherited, or they can pass to humans and other animals via contaminated meat or even surgical transplants. Prions are transmitted through meat when the animal being ingested (such as a cow) has the prion disease. After the cow's altered proteins (prions) enter the new host's body, they infect the new host in a similar manner.

Overview of Viruses that Affect HumansAnimal viruses cause a wide variety of diseases, many of which you have probably encountered, such as the common cold, the flu, the stomach flu, and pink eye. More serious diseases include severe acute respiratory syndrome (SARS), AIDS, Ebola hemorrhagic fever (EHF), and avian influenza.

Table 4.4 lists examples of human viruses and the diseases they cause. It focuses first on DNA viruses, and then on RNA viruses:

Table 4.4Examples of Human Viruses

DNA Viruses

Viral Family Viral Genera Example(s) Diseases or Conditions

Caused

Parvoviridae parvovirus human parvovirus fifth's disease

Adenoviridae adenovirus adenovirus respiratory infections and conjunctivitis (viral pink eye)

Papovaviridae papillomavirus human papillomavirus (HPV)

genital warts and cervical cancer

Poxviridae orthopoxvirus vaccinia virus smallpox

Herpesviridae

simplexvirus herpes simplex virus 1 (HSV-1), or human herpesvirus 1 (HHV-1)

cold sores (fever blisters)

simplexvirus herpes simplex virus 2 (HSV-2), or human herpesvirus 2 (HHV-2)

genital blisters

human herpesvirus 8

Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8 (HHV-8)

skin lesions and cancer

varicellovirus varicella-zoster virus (VZV), or human herpesvirus 3 (HHV-3)

chicken pox and shingles

human herpesvirus 4

Epistein-Barr virus (EBV), or human herpesvirus 4 (HHV-4)

infectious mononucleosis

DNA Viruses

Viral Family Viral Genera Example(s) Diseases or Conditions

Caused

Hepadnaviridae hepadnavirus hepatitis B virus (HBV)

hepatitis B (liver infection) and liver cancer

RNA Viruses

Viral Family Viral Genera Example(s) Diseases or Conditions

Caused

Picornaviridaerhinovirus common cold virus upper respiratory

tract infections

enterovirus poliovirus polio

Caliciviridae norovirus stomach flu virus 24–48 hour stomach flu

Togaviridae rubivirus rubella virus German measles

Flaviviridae hepatitis C virus hepatitis C virus hepatitis C (liver infection) and liver cancer

Coronaviridae coronavirus

SARS virus severe acute respiratory syndrome (SARS)

common cold virus upper respiratory tract infections

Rhabdoviridae lyssavirus rabies virus rabies

Paramyxoviridae paramyxovirus mumps virus mumps

Orthomyxoviridae orthomyxovirus influenza virus seasonal flu

Bunyaviridae hantavirus hantavirus hemorrhagic fever

Filoviridae Ebolavirus

Ebola virus hemorrhagic fever

Marburg virus hemorrhagic fever

Retroviridae lentivirus HIV AIDS

ConclusionViruses are relatively simple structures that cause a variety of diseases. Composed of proteins and nucleic acids, they lack the components of a classic cell, and because of this, they cannot make new viral particles, or virions, without the aid of a host cell. Viruses depend on the host cell for replication, a process they accomplish by invading the cell and hijacking its machinery.

Viruses contain either a DNA or RNA genome encased in a protein capsid, or shell. Some viruses enclose their capsid in a phospholipid envelope made out of the host cell's plasma membrane. The viral particle, or virion, tears away part of the membrane as it leaves the cell. The method by which viruses copy their genome varies depending on the type of nucleic acid they have. Viral genomes are limited, but are capable of directing the synthesis of new virions.

Some viruses, such as HIV, integrate into the host cell's genome, becoming a lifelong resident of the host. These types of viruses often take years to manifest themselves. Some integrated viruses can cause cancer, as in the case of HPV. We have effectively battled several viral diseases, such as smallpox and polio, with the use of vaccines. Others, such as HIV and HSV-1 and 2, still evade our attempts at elimination.

Are viruses living? This is a debate that has plagued the scientific and medical community for decades, and the answer depends largely on one's definition of  life. Although viruses are often referred to as being on the "edge of life," they have adapted to exploit host cells and to cause illness in a manner similar to that of living pathogenic organisms.

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