Mimivirus is a viral genus that contains the merely ascertained species Acanthamoeba polyphaga mimivirus ( APMV ) . The Mimivirus holds the largest mirid bug in diameter compared to the other known authoritative viruses like HIV or the influenza virus. Because of these characteristics, scientists had foremost mistaken the virus to be a bacteria. Mimivirus was foremost discovered in 1992 by a Gallic Scientist in Marseille. These scientists were look intoing Legionnaires ‘ disease, in which they came upon by accident, a “ coccus-like ” bacteria. It was n’t until 2003, when a diary was foremost published in find of the Mimivirus. The diary was written by a bacteriologist at the Universite de la Mediterranee in France, whom confirmed the designation of APMV. Mimivirus have a alone characteristic that is about similar to a bacteria on Gram staining ( Scola, 2003 ) . So the name Mimivirus, originates from its initial misidentification of a Gram-positive bacterium, therefore dubbed as the “ bug mimicking ” virus. The find of Mimiviruses contradicts the recognized theories of viruses being little in size and genome.


Mimiviruses are double-stranded DNA with a genome size of about 1.2 million base braces and 1018 protein coding cistrons including the new cistrons discovered late. The Mimivirus genome is round and belongs in the household Mimiviridae. Some scientists argue that the genome of Mimivirus is additive and NOT handbill, nevertheless there were no beginnings corroborating the conformation of the genome. Based on an negatron microscopy survey, the virions are nonenveloped icosahedrons with a diameter of 400-750 nanometer ( Kuznetsov, 2010 ) . Atomic force microscopy ( AFM ) is an imaging method with capablenesss of detecting little micro-organisms at a really high-resolution. This method was able to show the 20-icosahedral faces of the Mimivirus mirid bugs ( Xiao, 2009 ) . The Mimivirus contains an 80 nanometer filaments attached to the mirid bug and is classified as Baltimore categorization I.

Figure 1. Picture from: hypertext transfer protocol: //upload.wikimedia.org/wikipedia/commons/thumb/e/e1/Mimivirus.jpg/790px-Mimivirus.jpg

Mimivirus contains a coated bed of proteins on the icosahedral mirid bug that in some ways mimic the cell wall of Gram-positive bacteriums. This protein coat was believed to be a privacy to gull the ameboid host into thought that the virion is a bacteria, which causes the host to subject to eating its tiffin ( Claverie, 2009 ) . Scientists believed that the outer protein coat may function for another intent.

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Amoebas are considered a genus of Protozoa and obtain their nutrient ( algae, bacteriums, other protozoons, and bantam atoms of dead works or carnal affair ) via phagocytosis. This is of import to cognize because the Mimivirus infection is triggered by phagocytosis ( Ghigo, 2008 & A ; Monti, 2007 ) . First off, the Mimivirus has a strong resemblance towards Gram-positive bacteriums due to its big size and mimic abilities of Gram positive cell wall. Because of those features, the ameba, with no typical abilities, thought that the big virus was a bacteria and swallowed the virus via the mechanism of phagocytosis. Once the viral atom is absorbed by phagocytosis, a vacuole surrounds the viral atom and fuses to go a phagosome ( figure 2 ) . The captive viral atoms in the phagosome will so unify with the lysosome. The debasement from the lysosomal activity in the ameba will weaken the outer fiber bed, which will bring forth an gap of the five icosahedral faces on the vertex of the mirid bug ( Zauberman, 2006 and Xiao, 2009 ) . This allows the virus to let go of its Deoxyribonucleic acid to the host cell nucleus. From at that place, the Mimivirus reproduction will interrupt into three different zones known as the viral mill ( VF ) . The three VF zones are: ( 1 ) inner reproduction centre, ( 2 ) intermediate assembly zone, and ( 3 ) peripheral zone ( Monti, 2007 ) . The reproduction centre will bring forth viral proteins and the assembly zone will piece these proteins into mirid bugs. The peripheral zone will add the fibres to the mirid bug. Empty or filled DNA mirid bugs will so roll up near the cardinal nucleus, which will ensue in the formation of a big monolithic membrane, to which the host cell could non defy the big monolithic membrane and explosions ( procedure known to be amoebal lysis ) . The viral nucleocapsid DNA is released into the cell cytol ( Monti, 2007 ) . Future surveies of the Mimivirus may be linked with happening out its attachment stage and perchance a more in depth item on its written text factors.

Figure 2. Conventional representation of APMV reproduction rhythm ( Monti, 2007 ) . ( a1 ) Phagocytosis of viral atom. ( a2 ) Fusion of phagosome and lysosome, ( b3-b4 ) Virus releases DNA to host karyon ( c5 ) Mimivirus DNA came out the host karyon to organize the virus mill ( VF ) reproduction centre. ( d6 ) Replication centre produce viral proteins, assembly zone assembles mirid bugs, and peripheral zone adds the fibres, ( e7 ) Empty or DNA filled mirid bugs accumulate near the cardinal nucleus resulting in the formation of a big monolithic membrane. ( f8 ) Host cells could non defy the big monolithic membrane and explosions ( amoebal lysis ) , viral nucleocapsid DNA is released into the cell cytol.








The life rhythm of the Mimivirus in worlds is similar to amoebas, in that, entry is mediated via phagocytosis. Resources did non province how the virus attaches to, replicates, assemble, or released in the host. However, scientist had proposed that the Mimivirus could do farther incursion of the cytol by utilizing enzymatic activities necessary for the gap of the five icosahedral faces at the vertex of the mirid bug ( Zauberman, 2006 and Xiao, 2009 ) . Beginnings were non clear. The inquiry still remains whether or non see Mimivirus as a possible pneumonia agent. Some surveies had found dealingss correlating Mimivirus to pneumonia patients, but were diffident if the virus was the cause of the disease. See medical relevancy for more inside informations.


Recent surveies discovered a orbiter virus called “ Sputnik virophage. ” Satellite viruses are viruses that depend on the co-infection of the assistant virus in the host cell for its reproduction. The Sputnik is an icosahedral little virus ( 50 nanometer in diameter ) with 18.343 kilobits round dsDNA genome and uses the other virus ‘ machinery for reproduction. Probes of this little virus suggest that Sputnik can non reproduce in host ameba cells without the infection of Mimivirus. Sputnik reproduction occurs within the reproduction machinery of the Mimivirus VF.

Figure 3 shows Sputnik originating its reproduction rhythm utilizing Mimivirus as a assistant virus to perforate the host cell for entry. Once inside the host, Sputnik foremost travels to the viral mill created by the Mimivirus, and so occupy the Mimivirus VF to retroflex its ain genome. The ensuing viral messenger RNA would be translated in the host cytol. Sputnik proteins will so piece into viral atoms at the fringe of the Mimivirus mills and finally be released in the cell cytol via lysis. The effects this will hold on Mimivirus are that few of its ain viruses will be produced much lesser and that they will go distorted and less infective. There was besides grounds of a partial thickener of the mirid bug. Detailss of the reproduction were non provided.

Figure 3. Reproduction of traditional orbiter virus, Sputnik ( Claverie, 2011 ) . Following entry within the host cytol, Mimivirus and Sputnik goes separate ways. Mimivirus generates factors where the viral reproduction takes topographic point. Sputnik takes advantage of the Mimivirus VF zone for the reproduction of its genome to bring forth its transcripts. At the assembly phase, Sputnik requires the aid of Mimivirus.


The Mimivirus genome exhibits the same written text related nucleus cistrons as found in Poxviridae, proposing that the written text of some Mimivirus cistrons occurs in the cytol ( Raoult, 2004 ) . Mimivirus encodes a big figure of the constituents of its written text setup ( Legendre, 2011 ) . These constituents can be classified in four generic functional classs: protein interlingual rendition, DNA fix enzymes, chaperones, and new enzymatic tracts. Where these constituents play a function is another narrative. Mimivirus possesses 6 transfer RNA known to be three Leu, one Trp, one Cys, and one His. Functions and some cistron look of Mimivirus are still unknown, farther probes are presently preceded. Table 1 shows a list of cistrons found in the Mimivirus and its possible maps.

In add-on to these transfer RNAs, the Mimivirus besides exhibits proteins that maps in interlingual rendition. These are known to be aminoacyl-tRNA synthetases and interlingual rendition induction factor 4E ( e.g. mRNA cap binding ) ( Raoult, 2004 ) . Sources did non supply information on how or when Mimivirus use these proteins. Based on what was found, the two largest RNA polymerase II fractional monetary units are R501 and L244. The Mimivirus besides contains four smaller RNA polymerase II fractional monetary units: Rpb3/Rpb11 ( R470 ) , Rpb5 ( L235 ) , Rpb6 ( R209 ) , and Rpb7/E ( L376 ) . Functions of these RNA polymerase II are to catalyse the written text of DNA to synthesise precursors of messenger RNA. Again, it was non known when Mimivirus use RNA polymerase II. Mimivirus besides possesses a poly ( A ) polymerase ( R341 ) , and a series of written text factors such as L250, R339, R350, R429, R450, and R559.

Mimiviruses contains a few Deoxyribonucleic acid topoisomerases. These Deoxyribonucleic acid topoisomerases are enzymes in charge of work outing the web jobs associated with DNA reproduction, written text, recombination, and chromatin remodeling. R480, R194, and L221 are some illustrations of Deoxyribonucleic acid topoisomerases found in the Mimivirus.

Genomes can be damaged by chemical mutagens, UV ( UV ) light or ionising radiations ( Raoult, 2004 ) . The Mimivirus genome revealed several types of DNA fix enzyme, which in its ain purpose prevent Deoxyribonucleic acid mistakes. These include L315 and L720 cistrons, which serves as enzymes that locate and excise oxidized purines. Surveies besides suggest that the Mimivirus genome exhibits a UV-damage endonculease, which cleaves Deoxyribonucleic acid that was damaged by UV light off. Another Deoxyribonucleic acid fix enzyme is L359, which is involved in DNA mismatch fix and recombination ( procedure by which a nucleic acid is broken and so joined to a different one ) . L386 and R555 are in charge of fix for UV-induced DNA harm. Overall, Mimivirus appears unambiguously good equipped and prepared to mend DNA mismatch and amendss caused by oxidization, alkylating agent or UV visible radiation ( Raoult, 2004 ) . Due to this ability, Mimivirus atoms are therefore rather immune to inauspicious conditions. However, 15 proceedingss of 35 kilograys of irradiation with gamma beams or exposure of UV visible radiation would immediately kill the Mimivirus, despite their ability of DNA fix ( Raoult, 2004 ) .

Table 1. Majorly identified Mimivirus genome ( Raoult, 2004 ) . There are 1018 protein coding cistrons ( including the new cistrons discovered ) and 6 transfer RNA in the Mimivirus. This tabular array shows a list of cistrons found in the Mimivirus with its possible function and maps. dTDP = 3′-deoxy-thymidine-5 ‘ diphosphate ; ADP = adenosine 5’-diphosphate.

Mimivirus Newly Discovered Genes ( Legendre, 2011 ) . There are 1018 protein coding cistrons ( including the new cistrons discovered ) and 6 transfer RNA in the Mimivirus. This reveals some of the recent new 75 cistrons found in 2011, list of cistrons generated from the merger of antecedently identified ORFs, and list of deleted or renamed cistrons.


Pneumonia infections are sometimes unknown in 20 % -50 % instances around the universe ( La Scola, 2005 ) . However, some correlativities indicated that Mimivirus was associated with community and hospital-acquired pneumonia. Surveies have reported serologic grounds of APMV infection in 7.1 % – 9.7 % of patients with community acquired pneumonia ( La Scola, 2005 & A ; Berger, 2006 ) .

In the survey done by La Scola, 2005, serum samples of 376 Canadian patients with community-acquired pneumonia and 511 healthy control topics was tested to see if Mimivirus was the cause of infection. The control showed 12 people with the antibody for the Mimivirus, while 36 patients in the pneumonia infected group had antibodies to the Mimivirus, proposing that the survey had grounds back uping that Mimivirus is found in some instances of pneumonia. This survey does non demo that the Mimivirus is the cause for this infection. They were merely able to demo Mimivirus colonisation, but non the cause of infection. If Mimivirus is found to be the cause of pneumonia so more surveies should be done to happen out how to handle it. It besides raises inquiries on how effectual are human antibodies in halting the Mimivirus life rhythm.

Another survey done to research the consequence Mimivirus had on worlds is performed by Khan in 2007. Result showed that the Mimivirus could infect mammalian cells in laboratory conditions. In the survey, they inoculated grownup mice and found that they developed pneumonia within the scope of 3 to 7 yearss. The Mimivirus was introduced to the host mouse by an intracardiac path ( Khan, 2007 ) . The mouse was so tested for pneumonia by looking at the thickener of air sac walls. Khan concluded the survey, saying that the mice presented thick air sac walls, which supports the theory of Mimivirus links with pneumonia. While this survey showed mammalian cells could be infected, farther probes is needed to corroborate.

In another recent survey, antibodies against Mimivirus were found in patients with community-acquired pneumonia. These antibodies were detected utilizing microimmunofluorescence checks. It appeared that the virus was found more often in community-acquired than in control patients. The survey showed that patients with community-acquired pneumonia and serologic grounds of Mimivirus were more often re-hospitalized even after discharge. This was likely due to the deficiency of human antibodies in halting the Mimivirus. The survey suggests that Mimivirus is might be an etiologic agent of pneumonia that is acquired in establishments ( Standford University ) .

There is still really small known about what cells the Mimivirus onslaughts, which makes it hard to foretell the function of Mimivirus in the unknown causes of pneumonia. If Mimivirus does aim tissues in the lungs, as evidenced by the thickener of mouse air sac, so we may be able to understand the importance of these consequences in the medical field. Not adequate surveies have been conducted yet to find the Mimivirus infection, but the relationship between viral infection and human disease is worth researching since the causes of many pneumonia instances are still unknown.

Figure 5 ( Scola, 2005 ) . Mimivirus antigen is observed by scanning electronic microscopy. ( A ) Mimivirus antibody acknowledgment from the microimmunofluorescence check, ( B ) Mimivirus antibody acknowledgment from the Confocal microscope, ( C ) Mimivirus atoms in ameba are recognized by antibodies in the transmittal electronic microscopy. ( D ) Mimivirus atom size 400 nanometer in TEM.

Environmental RELEVANCE: Epidemiology

Probe of suspected Legionnaire ‘s pneumonia eruption in 1992 led to the isolation of a new micro-organism from a H2O chilling tower in West Yorkshire mill town of Bradford, England. Timothy Rowbotham, the officer in charge of Britain ‘s Public Health Laboratory Service, was look intoing the possible beginning of pneumonia eruption and by chance discovered the Mimivirus. A survey performed by Claverie et Al. 2009 revealed from an environmental DNA sample that there is an unexpected copiousness of big DNA viruses related to the Mimivirus within the marine environment ( Ghedin, 2005 & A ; Monier, 2008 ) . These Mimivirus related big DNA appears to be a important constituent in the ecology of micro- and pico- plankton populations throughout the oceans and likely in fresh H2O environments. It was besides suggested that these big DNA viruses may hold a important ecological impact through their ordinance of planktonic populations, and infection of omnipresent Marine invertebrates. There was besides some indirect grounds of Mimivirus links to marine invertebrates such as corals and sponges ( Caverie, 2009 ) . Following this line of thought a small farther, Claverie believed that some Mimiviridae may hold evolved to infect marine animate beings and trust on environmental phagocytosis as its chief nutrition system. Further probes on environmental relevancy are still needed.


Surveies done therefore far for the Mimivirus have involved genome sequencing and looking into its beginning. There were several serology surveies of worlds with clinical instances of pneumonia, which have shown a noticeable immune response to Mimiviruses, proposing current or old infection ; nevertheless there were besides other surveies that have NOT found any Mimivirus association with pneumonia patients ( Reynolds, 2010 ) . Because of this argument of these “ assorted research, ” consequences of Mimivirus began to raise uncertainty. If Mimivirus is found to be the cause of pneumonia so more surveies should be done to happen out how to handle it. Since, the correlativities are still a spot confusing ; scientists are non researching the interventions at the minute, at least non until these dealingss are cleared up.


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