Virus life cycle ppt

Four distinct modes of cell—cell transmission mechanisms have been described. First, cell—cell transmission is mediated by plasma membrane fusion between two cells. The viral capsids are transmitted from an infected cell to uninfected cells without being enveloped.

This mode of cell—cell transmission is described in retrovirus and herpesvirus. Second, cell—cell transmission occurs across a tight junction. Using viral entry receptors on the target cell, virions enter the uninfected target cells.

This mode of cell—cell transmission is described in herpesvirus and HCV. Third, cell-to-cell spread occurs across a neural synapse. Virions, either mature or incomplete naked core , assemble in either the postsynaptic or presynaptic cell depending on the virus, and either bud through the membrane into the synaptic space or are released from synaptic vesicles into the cleft.

Virions then either fuse directly with the opposing synaptic cells or are endocytosed. Rhabdovirus, herpes viruses, and paramyxoviruses move across neural synapses. Fourth, cell—cell transmission occurs across a virological synapse. Immune cells can be polarized via cell contact, which is termed an immunological synapse. A Via plasma membrane fusion. B Across tight junction. C Across a neural synapse. D Across a virological synapse. What is the advantage of cell—cell transmission?

It facilitates the viral spread from infected cell to uninfected neighboring cells via direct contact without diffusion. More importantly, the viruses associated with cells are physically protected from neutralizing antibodies. In fact, cell—cell transmission was uncovered by an experiment characterizing the neutralizing antibodies-resistant viral transmission. Notably, cell—cell transmission was found only in enveloped viruses, but not in naked viruses. Perhaps, cell—cell transmission is useless for naked viruses, where a bulk of virion is abruptly released upon cell lysis.

As stated above, most viruses enter the cell via receptor-mediated endocytosis. What would be the advantages of receptor-mediated endocytosis, as opposed to direct fusion? Unlike direct fusion, evidently, receptor-mediated endocytosis bypasses the actin cortex or the meshwork of microfilaments in the cortex that presents an obstacle for the penetration see Fig.

Moreover, by being taken up by endocytosis, animal viruses can avoid leaving the viral envelope glycoprotein on the plasma membrane, thus likely causing a delay in detection by immune system.

Typically, receptor-mediated endocytosis proceeds via a clathrin-dependent manner Fig. Receptor-mediated endocytosis is the mechanism intrinsic to the cells, which is utilized to take extracellular molecules into the cells. Clathrin -mediated 6 endocytosis, which is also the pathway utilized for uptake of LDL, is employed by many viruses, such as influenza virus and adenovirus. Upon the binding of the virus particle with the receptor, a clathrin-coated pit is formed, as clathrins are recruited near the plasma membrane.

Following the formation of an endocytic vesicle, the vesicles are fused with early endosomes. The virus particles are now located inside the early endosomes. Upon the binding of virus particles to the receptor, clathrins are recruited to form the clathrin-coated pit via its interaction with AP-2 adapter. Clathrin-coated pits are pinched off by dynamins.

After the vesicle coat is shed, the uncoated endocytic vesicle fuses with the early endosome. The capsids are released from the endosome by membrane fusion between viral envelope and endosome that is triggered by low pH inside the endosome. In addition to receptor-mediated endocytosis, a few other endocytic mechanisms are utilized by animal viruses Fig. For instance, caveolin -mediated 7 endocytosis is used for the entry of polyomaviruses, such as SV40 see Fig.

In this case, caveolin, instead of clathrin, serves as a coat protein; otherwise it is similar to clathrin-mediated endocytosis. Macropinocytosis 8 is utilized for the entry of particles with a larger size, such as vaccinia virus and herpes viruses. The virus particle first activates the signaling pathways that trigger actin-mediated membrane ruffling and blebbing. The formation of large vacuoles macropinosomes at the plasma membrane is followed by the internalization of virus particles and penetration into the cytosol by the viruses or their capsids.

Clathrin-mediated endocytosis. This pathway is the most commonly observed uptake pathway for viruses. The viruses are transported via the early endosome to the late endosome and eventually to the lysosome. The caveola pathway brings viruses to caveosomes. By the second vesicle transport step, viruses are transported to Golgi, and then to ER. Macropinocytosis is utilized for the entry of particles with larger size, such as vaccinia viruses and herpes viruses.

Following successful penetration inside cells, the virus particles need to get to an appropriate site in the cell for genome replication.

This process is termed intracellular trafficking. In fact, the biological importance of the cytoplasmic trafficking was not realized until the invention of live cell imaging technology.

For viruses that replicate in the cytoplasm, the viral nucleocapsids need to be routed to the site for replication. In fact, microtubule-mediated transport coupled with receptor-mediated endocytosis is the mechanism for the transport Fig. In addition, for viruses that replicate in the nucleus, the viral nucleocapsids need to enter the nucleus. For many DNA viruses, the viral nucleocapsids are routed to the perinuclear area via microtubule-mediated transport.

In this process, a dynein motor powers the movement of virus particles. As an analogy, the viral nucleocapsids can be envisioned as a train in a railroad. Two distinct viruses are used to explain how the entry is linked to cytoplasmic trafficking: A adenovirus naked and B herpes virus enveloped. Incoming viruses can enter cells by endocytosis A or direct fusion B. Following penetration into cytoplasm, either endocytic vesicles or viral capsids exploit dynein motors to traffic toward the minus ends of microtubules.

Either the endocytic vesicles A or the capsids B interact directly with the microtubules. The virus can also lyse the endocytic membrane, releasing the capsid into the cytosol A. As the virus particles approach to the site of replication, from the cell periphery to the perinuclear space, the viral genome becomes exposed to cellular machinery for viral gene expression, a process termed uncoating. Uncoating is often linked with the endocytic route or cytoplasmic trafficking see Fig.

For viruses that replicate in the nucleus, the viral genome needs to enter the nucleus via a nuclear pore. Multiple distinct strategies are utilized, largely depending on their genome size Fig.

For the virus with a smaller genome, such as polyomavirus, the viral capsid itself enters the nucleus. For viruses with a larger genome, the docking of nucleocapsids to a nuclear pore complex causes a partial disruption of the capsid eg, adenovirus or induces a minimal change in the viral capsid eg, herpes virus , allowing the transit of DNA genome into the nucleus.

A Polyomavirus capsids are small enough to enter the nucleus directly via the nuclear pore complex without disassembly. Uncoating of the polyomavirus genome takes place in the nucleus. B The adenovirus capsids are partially disrupted upon binding to the nuclear pore complex, allowing the transit of the DNA genome into the nucleus.

C For herpesvirus, the nucleocapsids are minimally disassembled to allow transit of the DNA genome into the nucleus. The viral genome replication strategies are distinct from each other among the virus families.

In fact, the genome replication mechanism is the one that defines the identity of each virus family. Furthermore, the extent to which each virus family relies on host machinery is also diverse, ranging from one that entirely depends on host machinery to one that is quite independent. However, all viruses, without exception, entirely rely on host translation machinery, ribosomes, for their protein synthesis. Exit can be divided into three steps: capsid assembly, release, and maturation.

The capsid assembly follows as the viral genome as well as the viral proteins abundantly accumulates. The capsid assembly can be divided into two processes: capsid assembly and genome packaging. Depending on viruses, these two processes can occur sequentially or simultaneously in a coupled manner. Picornavirus is an example of the former, while adenovirus is an example of the latter Fig. In the case of picornavirus, the capsids ie, immature capsid or procapsid are assembled first without the RNA genome.

Subsequently, the RNA genome is packaged or inserted via a pore formed in the procapsid structure. By contrast, in the case of adenovirus, the capsid assembly is coupled with the DNA genome packaging. Then, a question that arises is how does the virus selectively package the viral genome? A packaging signal , 9 a cis -acting element present in the viral genome, is specifically recognized by the viral capsid proteins, which selectively package either RNA or DNA.

A Sequential mechanism. For picornavirus, the procapsid, a precursor of the capsids, is preassembled without RNA genome. Subsequently, the RNA genome penetrates into the procapsid via a pore. B Coupled mechanism. For adenovirus, the DNA genome is packaged into the capsid during capsid assembly. For naked viruses, the virus particles are released via cell lysis of the infected cells.

Thus, no specific exit mechanism is necessary, because the cell membrane that traps the assembled virus particles are dismantled. Examples of naked viruses are polyomavirus ie, SV40 and adenovirus. By contrast, in cases of enveloped viruses, envelopment , a process in which the capsids become surrounded by lipid bilayer, takes place prior to the release. With respect to the relatedness of the capsid assembly to the envelopment, two mechanisms exist.

First, the envelopment can proceed after the completion of capsid assembly Fig. In this sequential mechanism, the fully assembled capsids are recruited to the membrane by interaction of the viral capsids with viral envelope glycoprotein.

Examples of this include herpesvirus and hepatitis B virus. Alternatively, the envelopment can occur simultaneously with the capsid assembly Fig. Retrovirus is the representative of this coupled mechanism.

The capsid assembly occurs prior to the envelopment. The assembled capsid is then targeted to the membrane for envelopment. Togavirus constitutes a family of positive-strand RNA viruses see Table Capsid proteins and the viral genome are recruited together to the budding site on the membrane.

Capsid assembly and the envelopment of the capsid proceeds simultaneously. The envelopment process can be divided into three steps: a bud formation, a bud growth, and finally membrane fusion. On the other hand, regarding the membrane for envelopment, two cellular membranes are exploited. The plasma membrane is the site of envelopment for some viruses, such as retrovirus and influenza virus, whereas endosomes, such as endoplasmic reticulum ER and Golgi bodies, are the site of envelopment for others, such as herpesvirus see Fig.

Then, how are the viruses released from the infected cells? Most enveloped viruses are released extracellularly via exocytosis 10 ; often, this process is also called budding , as an analogy of buds in plants.

Via budding, the envelopment proceeds in a linked manner with extracellular release. Then a question that arises is how mechanistically is budding triggered?

The clue for this was revealed by the identification of a peptide motif termed late L domain , 11 which is instrumental in triggering the budding process Box 3. Briefly, Gag protein, via its late domain, recruits cellular factors involved in the multivesicular bodies 12 MVBs pathway and subverts the MVB pathway for budding.

Although the replicative life cycle of viruses differs greatly between species and category of virus, there are six basic stages that are essential for viral replication.

Attachment: Viral proteins on the capsid or phospholipid envelope interact with specific receptors on the host cellular surface. This specificity determines the host range tropism of a virus.

Penetration: The process of attachment to a specific receptor can induce conformational changes in viral capsid proteins, or the lipid envelope, that results in the fusion of viral and cellular membranes. Some DNA viruses can also enter the host cell through receptor-mediated endocytosis. Uncoating: The viral capsid is removed and degraded by viral enzymes or host enzymes releasing the viral genomic nucleic acid.

Replication: After the viral genome has been uncoated, transcription or translation of the viral genome is initiated. It is this stage of viral replication that differs greatly between DNA and RNA viruses and viruses with opposite nucleic acid polarity. This process culminates in the de novo synthesis of viral proteins and genome.

Assembly: After de novo synthesis of viral genome and proteins, which can be post-transrciptionally modified, viral proteins are packaged with newly replicated viral genome into new virions that are ready for release from the host cell. This process can also be referred to as maturation. Virion release: There are two methods of viral release: lysis or budding. Lysis results in the death of an infected host cell, these types of viruses are referred to as cytolytic. Influenza A viruses primarily cause respiratory tract infections in mammals and birds.

The virus emerged in China in the winter of and spread rapidly worldwide via ships, aeroplanes, and trains. All 16H and 9N subtypes recognized currently have been recorded in birds in most possible combinations. It is a tricyclic amine. In poultry, low pathogenicity strains typically cause respiratory signs. Example of an Influenza Virus Naming.

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The structure of the … which has different roles in the life cycle of the virus. This service is similar to paying a tutor to help improve your skills. The virus localizes and replicates in various target organs, for example, local lymph nodes and the liver.

Most commonly used methods are protein methods, immunostaining methods, nucleic acid methods. Attaches to cell by tail fibers. Stages of poliovirus pathogenesis. The diagram illustrates multiple steps of poliovirus pathogenesis, starting from virus entry through oropharynx fecal—oral transmission , virus multiplication at the … … Emergence of Influenza An agent of great concern globally is influenza virus.

About Flu. Several host cell … If you continue browsing the site, you agree to the use of cookies on this website. The H1N1 and H3N2 influenza virus subtypes are the most prevalent in humans and account for several pandemics, including the H1N1 pandemic that caused worldwide mortality and morbidity in the recent past [].

The earliest reports of a coronavirus infection in animals occurred in the late s, when an acute respiratory infection of domesticated chickens emerged in North America. Over the past decade, this was supported by numerous screening approaches, which identified cellular factors relevant for intracellular virus … Influenza Influenza is caused by RNA viruses of the family Orthomyxoviridae, the influenza viruses.

Depending on the type of nucleic acid, cellular components are used to replicate the viral genome and synthesize viral proteins for assembly of new virions. These signatures will aid in the rational development, testing, and evaluation of novel vaccines and will allow evaluation of the effect of … The increasing geographic spread of Hyalomma ticks, which are responsible for viral transmission widespread, threatens billions of people. WHO works with governments and partners across the Region to promote health, keep the world safe, and serve the vulnerable.

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