Is every part of a virus important for replication?

Is every part of a virus important for replication?

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Is every component of a virus absolutely essential for its infection and replication in a host cell? Or can you just have parts of it to cause infection?

Unless you have a specific virus in mind, I can speak generally about viruses. It seems that the viral genome is reduced to just essential genes. Many viruses segregate their genome into periods of expression: early, mid and late. The early proteins are so-called because they encode for proteins that help their entry into cells (what is called infection). Middle and late genes tend to help the virus co-opt cellular machinery to aid in viral replication. Late genes are then useful for final stages of viral assembly and ultimtely their exit from the cell (lysis) and the newly made viral particles can go on and infect more cells. When viewed in this manner, it follows that removing even one coding region from the viral genome would inhibit the overall infection/reproduction/assembly process. In fact, if you remove the gene encoding for a viral envelope protein, purified virus added to cells in culture are able to infect cells, but not produce complete and functional viral particles. In this sense, they are infection-competent, but reproduction-incompetent.

HIV has nine genes. According to the paper cited below, three of these genes (vpu, vpr and nef) are not required for replication in cultured cells.

Gibbs JS et al. (1994) Construction and in vitro properties of HIV-1 mutants with deletions in "nonessential" genes. AIDS Res Hum Retroviruses 10: 343 - 50

Auxiliary genes that are not essential for viral replication in cell culture are found in all known lentiviruses. The "nonessential" auxiliary genes of HIV-1 are vif, vpr, vpu, and nef. Sequences within the upstream region of U3 in the LTR are also not required for virus replication in cell culture. We constructed a panel of 23 mutants with single and combination deletions in these regions in the wild-type HIV-1 infectious molecular clone NL4-3. Deletion of the vpu, vpr, and nef genes and the U3 upstream sequence (US), individually or in combinations, did not appreciably alter virus replication in either chimpanzee PBMCs, human PBMCs, or in the B/T cell hybrid line CEMx174. In contrast, deletion of the vif gene dramatically delayed virus replication in all three cell types. This collection of HIV-1 deletion mutants will be useful for elucidating the functions of these genes and for investigating antiviral immunity in animal models.

(PBMC = peripheral blood mononuclear cell)

As might be expected, none of these genes encodes a component of the virus - they are regulatory genes involved in co-ordinating the infective cycle of the virus. They are however implicated in HIV-associated disease symptoms. According to the Los Alamos National Laboratory HIV Sequence Compendium 2008:

vpu is an integral membrane protein which promotes extracellular release of viral particles and degrades CD4 in the ER.

vpr promotes nuclear localization of the preintegration complex, inhibits cell division, and arrests infected cells at G2/M

nef downregulates CD4 and class I MHC

Virus Infections and Hosts

Viruses can be seen as obligate, intracellular parasites. A virus must attach to a living cell, be taken inside, manufacture its proteins and copy its genome, and find a way to escape the cell so that the virus can infect other cells. Viruses can infect only certain species of hosts and only certain cells within that host. Cells that a virus may use to replicate are called permissive . For most viruses, the molecular basis for this specificity is that a particular surface molecule known as the viral receptor must be found on the host cell surface for the virus to attach. Also, metabolic and host cell immune response differences seen in different cell types based on differential gene expression are a likely factor in which cells a virus may target for replication. The permissive cell must make the substances that the virus needs or the virus will not be able to replicate there.

How is the CoV genome organized?

There are several sections of the CoV genome, known as open reading frames (ORFs), that serve as the instructions for making CoV proteins. All CoVs have two, really long ORFs that are translated into equally long “polyproteins,” which are then cut up to make 16 individual, non-structural proteins. These nonstructural proteins are responsible for basic but highly important functions that mostly involve viral RNA synthesis. All CoVs also have an additional 4 ORFs for making the structural proteins of the virus: spike (S), envelope (E), membrane (M), and nucleoprotein (N). There are other proteins that CoV genomes can encode, but this can differ depending on the specific CoV species.

CoV Genome Organization. Download the PDF version in the “Save & Share” tab.

Reproduction in Viruses (Replication of viruses)

Viruses are obligate intracellular parasite. They are reproduced only within a host cell. Viruses lack the enzyme for its replication. It uses the metabolic machinery of the host for its replication. Isolated viruses are only protein-coated particles. They are transmitted from one host cell to another.

Each type of virus infects only a limited range of hosts. It is called its host range. Viruses identify their host by a lock-and-key. There are specific receptor molecules on the host cells. Similarly, some proteins are present on surface of the virus. These receptors and proteins are involved in lock and key attachment. Some viruses have broad host ranges. They infect on several species of host. For example, rabies virus can infect number of specks. Some species have narrow host range. They infect only single specie. For example, phage virus infects only E. coll.

There are following stages of infection and replication of viruses:

1. Penetration: It is the first step of infection. Mechanism of penetration is different in different species. For example, phage uses their tail apparatus to inject DNA into a bacterium. Their tails have special enzyme lysozyme. It breaks the cell wall and cell membrane of bacterium. In some cases, complete virion enters into the host like AIDS virus.

Fig: GesenrUzed reproductive cycle of viruses

2. Replication: Viral DNA controls the metabolic machinery of the hos . It reprugranunes the viral genes and manufactures its capsids. Most DNA viruses use DNA polymerase of the host cell

to synthesize its new DNA. RNA viruses contain their own enzymes to initiate replication within the host. Host has no enzyme to copy RNA.

The virus uses resources of host for viral production. Host provides the nucleotides for nucleic acid synthesis. Virus uses its enzymes, rioosomes, tRNAs, amino acids and other machinery.

  1. Assembly of virion: Viral nucleic acid molecules and capsids are produced. Their assembly into new viruses is a spontaneous process. This process is called self assembly. RNA and capsomeres of TMV can be separated in the laboratory. If its contents are mixed it spontaneously reassemble itself.
  2. Release of virions: Hundred or thousands of viruses emerge from host cell. The host cell is often destroyed in the process. The destruction of host cells causes some symptoms of viral diseases. For example, colds and influenza viruses destroy the mucous membrane in respiratory passages. It causes symptoms of cold and influenza. The newly formed viruses infect other cells and in this way a new cycle started.

Variations in the reproductive cycles of viruses

Many var: ‘dons are present in the basic mechanism of reproductive cycle of animal and plant viruses:

(a) Animals viruses

1. Viruses without envelop: Its example is phage virus. Phage virus

attack on bacteria E. coli. It has simple mechanisr of penetration and replication. But it has two cycles of infection’

(a)Lytic cycle: In this case, bacteria burst arid release a large number of phage.

(b)Lysogenic cycle: In this case, bacteria do not burst. Viral

DNA incorporates in the bacterial DNA as prophage. It remains their in inactive form and replicates with the replication of bacterial DNA. Sometimes, it comes out during process of induction and start lytic cycle.

2. Viruses with envelopes: Several viruses have external envelopes. These envelopes are derived from the host cells. The envelops have glycoprotein spikes. These viruses attach on their host receptors with the help of these spikes. Viral envelope fuse with plasma membrane of host and capsid and viral genome enters into the host cells. After that replication start. New viruses develop new nucleic acids, capsids and spike. They stimulate the

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endoplasmic reticulum of host cell to synthesize new envelopes. The viruses budded off from the surface of host cells. Some viruses like Herpes virus derives their envelops from the nuclear membrane of host cell.

  1. Retroviruses: Retroviruses are RNA viruses. Their RNA enters into the host cells. It is changed into DNA by an enzyme reverse transcriptasc. This viral DNA incorporates in host DNA as provirus. Now it is part of host DNA. It synthesizes new RNA and new capsids new enzymes. Thus many new virions are formed. These virions develop envelops and budded off from the host cells.
  2. Plant viruses: Most plant viruses are RNA viruses. Most of them have rod shaped capsid like TMV. There are two methods of infection of plant viruses:

(a)Horizontal transmission: In this case, virus infection spread from external source to plant. It may spread from leaves to leaves.

(b)Vertical transmission: In this case, viruses are transferred from one plant to •other plants by asexual propagation and infected seeds.

Life Cycle of Phage Virus

The Bacteriophage or phage virus replicates only inside the bacterial cell. Phage virus shows two types of cycles during its replication: Lytic and lysogenic cycles.

Lytic Cycle of Phage Virus

The phage virus causes the lysis of the bacteria in the lytic cycle. Such viruses are called lytic or virulent phage. Lytic cycle is divided into following steps:

the receptor site on the cell wall of the bacterium. Weak chemical union takes place between the virus and the receptor site.

  1. Penetration: The tail of virus releases lysozyme enzyme. It dissolves a small part of the bacterial cell wall. The tail sheath contracts and pushes the tail core into bacteria through its cell wall and cell membrane. The virus injects its DNA in to the bacterial cell like syringe. The protein coat (tail and head) of the virus remains outside the bacterial cell. However, many animal viruses enter the host as a whole. •
    1. Multiplication: The viral DNA starts controlling the biosynthetic machinery of the bacteria inside the bacterial cell. It induces the bacterial cell to synthesize the parts of the virus, protein and DNA. Then virus multiplies to form many new viruses. Approximately 200 new viruses are formed after 25 minutes of the infection.
    2. Lysis: Many viruses are formed in the bacteria. The bacterial cell undergoes lysis and bursts. The newly formed viruses are released and infect other bacteria.

    Lysogneic Cycle

    Lysogenic cycle

    The phage does not always destroy bacteria. Sometimes, it lives peacefully inside the bacterial cell. It does not control the biosynthetic machinery of the host bacteria. The viral DNA incorporated into the bacterial chromosome. The phage in this state is called Proghage. This process is called lysogeny. The bacteria continue to live and reproduce normally in this condition. The viral DNA becomes the part of the bacterial chromosome. It passes to

    each daughter cell in all coming generations.

    Sometimes, the viral DNA detaches from the bacterial chromosome and starts lytic cycle. This process is called induction. The lysogenic bacteria are resistant to viral infection by same or similar phage virus. The phage which causes lysogeny is called temperate or lysogenic phage.

    The phage posses a gene code for repressor protein. This protein represses the replication of phage DNA in lysogenic cycle. Repressor proteins save the bacteria from lysis.

    The Lytic Cycle

    The lytic cycle is the faster of the two cycles a virus can take when replicating itself.

    During this cycle, the virus’ genetic material “hi-jacks” the cell and starts using it’s resources to create more copies of itself. It replicates itself in different parts (e.g. replicates its DNA/RNA, replicates its capsid, etc).

    Once the virus has created many copies of its different parts, the virus reassembles all of its parts. It does so until the entire cell is filled to the brim, until it explodes (or if you’re fancy — until it “lyses”) and releases itself back into the host body to go infect more cells.

    As you can imagine, this process of infection grows exponentially fast. For every one cell that gets infected, hundreds to thousands more can get infected after it undergoes a lytic cycle.


    ⇒ Genetic information for viral replication is contained in the viral nucleic acid but lacking the biosynthetic enzymes.

    ⇒ The virus depends on the synthetic machinery of the host cell for replication.

    ⇒ The viral multiplication cycle can be divided into six sequential phases as:-

    • Adsorption or Attachment
    • Penetration
    • Uncoating
    • Biosynthesis (Replication & Protein synthesis)
    • Maturation or Assembly
    • Release


    • Virions may come into contact with cells by random collision but adsorption takes place only if there is an affinity between host cell and virus.
    • The cell surface should contain specific receptor sites to which the virus can gain attachment.
    • For e.g. – in HIV the attachment is between the CD4 receptor on the host cells and viral surface glycoprotein gp 120.


    • Animal cells do not have rigid cell wall & the whole virus can enter into them.
    • Virus particles may be engulfed by a mechanism resembling phagocytosis, a process known as “viropexis”.
    • In enveloped viruses, the viral envelope may fuse with the plasma membrane of the host cell & release the nucleocapsid into the cytoplasm.


    • A process in which the outer layer and capsid of a virus is removed, leading to the release of viral genetic material into the host cell.
    • In most of the viruses, Uncoating is affected by the action of lysosomal enzymes of the host cells.
    • After Uncoating viral nucleic acid incorporates itself into host cell’s genetic material.


    • This phase includes the synthesis not only of viral nucleic acid & capsid protein but also of enzymes necessary in various stages of viral synthesis, assembly, and release.
    • Steps in Biosynthesis:-
    • Transcription of messenger RNA (mRNA) from the viral nucleic acid. This process is called as “Early Transcription”.
    • Translation of the mRNA into “early proteins”. These Early protein are enzymes which initiate and maintain the synthesis of virus components. This process is called as “Early Translation”. They may also shut down the synthesis of host protein & nucleic acid.
    • Replication of viral nucleic acid. In this process, the viral genome is multiplied for the synthesis of new Virions.
    • Transcription of mRNA (Late Transcription) and then the formation of proteins called as ‘late’ or structural proteins (Late Translation). These proteins are the components of daughter virion capsids.


    • Maturation consists of the Assembly of daughter Virions which takes place after the formation of viral nucleic acid and proteins.
    • Virion assembly may take place in the host cell nucleus (e.g. Herpes & Adenovirus) or cytoplasm (e.g. Picorna & Poxvirus).
    • At this stage, the non-enveloped viruses are present intracellularly as fully developed virions, but in case of enveloped viruses, only the nucleocapsid is complete.
    • Envelopes are derived from the host cell membrane during the process of The host cell membrane which becomes the envelope is modified by incorporation of virus-specific antigen.


    • In human viruses, the release of progeny virions usually occurs without cell lysis.
    • Progeny virions are released into the surrounding medium and may infect other cells via budding.
    • In some viruses (e.g. varicella), transmission occur directly from cell to cell, the very little free virus being demonstrable extracellularly in the medium.
    • Some of the human viruses cause profound damage to the host cell & may be released by cell lysis (e.g. poliovirus).

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    How the coronavirus hijacks human cells to spread itself

    You are free to share this article under the Attribution 4.0 International license.

    Researchers have discovered a method the coronavirus uses to manipulate human cells to ensure its own replication.

    This knowledge will help develop drugs and vaccines to fight the coronavirus.

    A virus takes control of an infected cell because every virus depends on the resources and molecular machines of the cell to multiply. This also applies to SARS-CoV-2, the virus that has caused the COVID-19 pandemic.

    In a new study, researchers discovered a mechanism the coronavirus uses to favor the production of its proteins over infected cells’ own. The mechanism leads to cells greatly reducing the production of their own proteins, instead producing almost only viral proteins.

    This not only boosts the production of new viruses, but also inhibits the immune response against the coronavirus infection.

    After the virus has entered a human cell during a SARS-CoV-2 infection, the viral protein NSP1 is produced as one of the first viral proteins. Researchers already knew from other coronaviruses that NSP1 inhibits the production of the infected cell’s own proteins, but it wasn’t yet clear how this occurs.

    The new work clarifies how NSP1 inhibits cellular protein production.

    Ribosomes are the cellular machines that produce proteins. They read the blueprint, the messenger RNA, for a given protein and assemble the amino acids in the corresponding order. During reading, the messenger RNA passes through a channel on the ribosome.

    The researchers found that NSP1 binds to this channel and blocks the ribosome. Using cryo-electron microscopy, they found they could see the binding site of NSP1 in the ribosome channel at atomic resolution.

    “This detailed image provides important information for potential design of a drug that can prevent NSP1 binding without interfering with ribosomal function. If NSP1 can no longer interact with the ribosome, this allows activation of cellular defense systems that can stop viral replication,” explains coauthor Nenad Ban, professor for molecular biology at ETH Zurich.

    Using biochemical and cellular experiments, the researchers were able to show that NSP1 alone is sufficient to inhibit protein production. Based on the detailed picture of the binding mode of NSP1, the researchers were able to produce modified NSP1 variants that have lost their inhibitory effect.

    SARS-CoV-2 viruses with these inactive variants of the NSP1 protein will likely be attenuated, meaning they can no longer cause severe disease. Attenuated viruses can potentially be used as a vaccine. Many other vaccinations against viral diseases are already based on this principle.

    The researchers were also interested in the question of why the viral proteins are produced in large quantities despite the inhibition of ribosomal function by NSP1. They found out that the viral RNA has unique properties because of which it is read very efficiently by ribosomes compared to cellular messenger RNAs.

    “By NSP1 blocking ribosomes, functional ribosomes become scarce and at the same time viral RNA can make up almost half of the total RNA in the cell. Under these conditions, the viral RNA is preferentially read from the still functional ribosomes compared to the cell’s own messenger RNA,” explains coauthor Oliver Mühlemann, professor of biochemistry at the University of Bern.

    The researcchers will continue to work to gain further insights into how SARS-CoV-2 manipulates the cell in its favor.

    All three participating research groups are part of the National Center of Competence in Research (NCCR) RNA & Disease, which the Swiss National Science Foundation as well as the University of Bern and ETH Zurich fund. The research appears in Nature Structural & Molecular Biology.

    Researchers develop technique to track yellow fever virus replication

    The liver of a mouse whose immune cells lack the immune signaling component known as STAT1 shows severe lymphocyte infiltration and inflammation, as well as necrosis, after infection with YFV-17D. Credit: Florian Douam and Alexander Ploss, Princeton University

    Researchers from Princeton University's Department of Molecular Biology have developed a new method that can precisely track the replication of yellow fever virus in individual host immune cells. The technique, which is described in a paper published March 14 in the journal Nature Communications, could aid the development of new vaccines against a range of viruses, including Dengue and Zika.

    Yellow fever virus (YFV) is a member of the flavivirus family that also includes Dengue and Zika virus. The virus, which is thought to infect a variety of cell types in the body, causes up to 200,000 cases of yellow fever every year, despite the widespread use of a highly effective vaccine. The vaccine consists of a live, attenuated form of the virus called YFV-17D, whose RNA genome is more than 99 percent identical to the virulent strain. This one percent difference in the attenuated virus' genome may subtly alter interactions with the host immune system so that it induces a protective immune response without causing disease.

    To explore how viruses interact with their hosts, and how these processes lead to virulence and disease, Alexander Ploss, assistant professor of molecular biology, and colleagues at Princeton University adapted a technique—called RNA Prime flow—that can detect RNA molecules within individual cells. They used the technique to track the presence of replicating viral particles in various immune cells circulating in the blood of infected mice. Mice are usually resistant to YFV, but Ploss and colleagues found that even the attenuated YFV-17D strain was lethal if the transcription factor STAT1, part of the antiviral interferon signaling pathway, was removed from mouse immune cells. The finding suggests that interferon signaling within immune cells protects mice from YFV, and that species-specific differences in this pathway allow the virus to replicate in humans and certain other primates but not mice.

    Accordingly, YFV-17D was able to replicate efficiently in mice whose immune systems had been replaced with human immune cells capable of activating interferon signaling. However, just like humans immunized with the attenuated YFV vaccine, these "humanized" mice didn't develop disease symptoms when infected with YFV-17D, allowing Ploss and colleagues to study how the attenuated virus interacts with the human immune system. Using their viral RNA flow technique, the researchers determined that the virus can replicate inside certain human immune cell types, including B lymphocytes and natural killer cells, in which the virus has not been detected previously. The researchers found that the panel of human cell types targeted by the virus changes over the course of infection in both the blood and the spleen of the animals, highlighting the distinct dynamics of YFV-17D replication in the human immune system.

    The next step, said Florian Douam, a postdoctoral research associate in the Department of Molecular Biology and first author on the study, is to confirm YFV replication in these subsets of immune cells in YFV-infected patients and in recipients of the YFV-17D vaccine. Viral RNA flow now provides the means to perform such analyses, Douam said.

    The researchers also plan to study whether the virulent and attenuated strains of yellow fever virus infect different host immune cells. The approach may help explain why some people infected with the virus die while others develop only the mildest of symptoms, as well as which changes in the YFV-17D genome weaken the virus' ability to cause disease. "This could guide the rational design of vaccines against related pathogens, such as Zika and Dengue virus," Ploss said.

    More information: Nature Communications, DOI: 10.1038/NCOMMS14781


    The Papillomaviridae is a family of small, non-enveloped viruses with double stranded DNA genomes of 5,748 bp to 8,607 bp (Table 1. Papillomaviridae). Their classification is based on pairwise nucleotide sequence identity across the L1 open reading frame. Members of the Papillomaviridae primarily infect mucosal and keratinized epithelia, and have been isolated from fish, reptiles, birds and mammals. Despite a long co-evolutionary history with their hosts, some papillomaviruses are pathogens of their natural host species.

    Table 1.Papillomaviridae. Characteristics of members of the family Papillomaviridae.



    human papillomavirus 16 (K02718), species Alphapapillomavirus 9, genus Alphapapillomavirus, subfamily Firstpapillomavirinae

    Non-enveloped, 55 nm, icosahedral

    Circular dsDNA. Genome varies from 5,748 bp to 8,607 bp.

    Bidirectional theta replication

    Early and late transcripts, alternative splicing, alternative open reading frames

    Mammals, reptiles, birds, and fish

    Two subfamilies include >50 genera and >130 species


    any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as &ldquofiltrable&rdquo because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living host cell. Because these properties are shared by certain bacteria ( rickettsiae, chlamydiae ), viruses are now characterized by their simple organization and their unique mode of replication. A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope.

    Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle ( virion ) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.

    Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat) there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.

    Because host cells do not have the ability to replicate &ldquoviral RNA&rdquo but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme ( transcriptase ) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.

    In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.

    Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses &ldquosteal&rdquo their lipid envelope from the host cell, virtually all of them produce &ldquoenvelope proteins&rdquo that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.

    Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses , it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses , actually enter a time known as &ldquoviral latency,&rdquo when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.

    In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon . Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response . Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells .

    Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses , which are called proviruses before and after integration of viral DNA into the host genome.

    Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the human immunodeficiency virus , appear to be actively toxic, but those are the exception, not the rule.

    However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis induction of cell proliferation (as in certain warts and molluscum contagiosum ) formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus and perhaps most importantly, symptoms caused by the host's immune response , such as inflammation or the deposition of antigen-antibody complexes in tissues.

    Because viral reproduction is almost completely carried out by host cell mechanisms, there are few points in the process where stopping viral reproduction will not also kill host cells. For this reason there are no chemotherapeutic agents for most viral diseases. acyclovir is an antiviral that requires viral proteins to become active. Some viral infections can be prevented by vaccination (active immunization ), and others can be treated by passive immunization with immune globulin , although this has been shown to be effective against only a few dozen viruses.