A viroplasm is an inclusion body in a cell where viral replication/assembly occurs. They may be thought of as viral factories in the cell. Very little is understood about the mechanism of viroplasm formation. These appear electron-dense under the electron microscope, most likely due to high amounts of viral RNA in them.

Viroplasm has been found in the cauliflower mosaic virus,[1] rotavirus,[2] vaccinia virus[3] and the rice dwarf virus.[4]


A Viroplasm is a perinuclear or a cytoplasmic large inclusion where viral replication and assembly occur.[5] Viral products and cell elements are confined in viroplasms.[5] The viroplasm formation seems to be caused by the interactions between the virus and the infected cell.[5] There are many viroplasms in one infected cell. Viroplasms appear dense to electron microscopy, they are insoluble.[5]

Synonymous : viral factory, electron-dense inclusion

Groups of viruses that form viroplasms

Viroplasms have been reported in many unrelated groups of Eukaryotic viruses that replicate in cytoplasm, however, viroplasms from plant’s viruses have been less investigated than viroplasms from animal’s viruses.[5]

A high number of other viruses most probably form viroplasms as well, but they are not described or discovered yet.

The viroplasm : structure and formation

Viroplasms are localized in the perinuclear area or in the cytoplasm of infected cells. Viroplasms are formed early in the infection cycle.[5][14] The number and the size of viroplasms depend of the virus, the virus isolate, hosts species, and the step of infection.[15] For example, viroplasms of mimivirus have a similar size as the size of the nucleus of its host, the amoeba Acanthameba polyphaga.[8] They alter large areas of the infected cells and induce changes in composition and organization of cellular compartments depending on the step of the virus replication cycle. This process involves a number of complex interactions and signaling events between viral and cell factors.

Viroplasms are formed early during the infection, there is an exclusion of host proteins and organelles from the region where the factory will be assembled. At the same time, large amounts of viral structural proteins and viral mitochondria seem to provide the energy required for viral replication, protein synthesis and assembly. The virus factory is often enclosed by a membrane (often derived from the rough endoplasmic reticulum) or by cytoskeletal elements.[5][14]

In animal cells, virus particles are gathered by the [5][16] MTOCs are not found in plant cells. Plant viruses induce the rearrangement of membranes structures to form the viroplasm. This is mostly shown for plant RNA viruses.[14]


Viroplasms are places where the viral replication and assembly take place.[5] These structures concentrate viral components required for the genome replication and the morphogenesis of new virus particles. This wrapping increases the efficiency of these processes.[5] These subcellular domains could also protect viral complexes from the cellular degradation machinery and the viral RNA from silencing. But the viroplasm can also protect host cells and prevent the virus propagation by stocking viral products in a subcellular domain meanwhile the degradation of them by proteases and nucleases.[14]

In the case of the Cauliflower mosaic virus (CaMV), viroplasms improve the virus transmission by the aphid vector. Viroplasms control release of virons when the insect stings an infected plant-cell or a cell near the infected cells.[13]

Viroplasm : product of the coevolution between virus / host ?

Aggregated structures may protect viral functional complexes from the cellular degradation machinery. For example, formation of viral factories of the ASFV viroplasm is very similar to the aggresome formation.[5] An aggresome is a perinuclear site where misfolded proteins are transported and stored by the cell components meanwhile their destruction. The viroplasm could be the product of a coevolution between the virus and its host. It’s possible that a cellular response originally designed to reduce the toxicity of misfolded proteins is exploited by cytoplasmic viruses to improve their replication, the capsid synthesis and the assembly.[13] Alternatively, the activation of host defense mechanisms may involve sequestration of virus components in aggregates to prevent their dissemination, followed by their neutralisation. For example, viroplasms of mammalian viruses contain certain elements of the cellular degradation machinery which might enable cellular protective mechanisms against viral components.[17] Given the co-evolution of viruses with their host cells, changes in cell structure induced during infection are likely to involve a combination of the two strategies.[5]

Use in diagnostic

Presence of viroplasms is used to diagnostic certain viral infections. Understanding the phenomenon of virus aggregation and of the cell response to the presence of virus, and whether viroplasms facilitate or inhibit virus multiplication, may help to develop new therapeutic approaches against virus infections in animal and plant cells.[14]


  1. ^ Xiong; Muller, S; Lebeurier, G; Hirth, L (1982). "Identification by immunoprecipitation of cauliflower mosaic virus in vitro major translation product with a specific serum against viroplasm protein". The EMBO Journal 1 (8): 971–976.  
  2. ^ Nilsson; Von Bonsdorff, CH; Weclewicz, K; Cohen, J; Svensson, L (1998). "Assembly of viroplasm and virus-like particles of rotavirus by a Semliki Forest virus replicon". Virology 242 (2): 255–65.  
  3. ^ Szajner; Weisberg, AS; Wolffe, EJ; Moss, B (2001). "Vaccinia virus A30L protein is required for association of viral membranes with dense viroplasm to form immature virions". Journal of Virology 75 (13): 5752–61.  
  4. ^ Wei; Kikuchi, A; Suzuki, N; Shimizu, T; Hagiwara, K; Chen, H; Omura, T (2006). "Pns4 of rice dwarf virus is a phosphoprotein, is localized around the viroplasm matrix, and forms minitubules". Archives of Virology 151 (9): 1701–12.  
  5. ^ a b c d e f g h i j k l m n o Novoa RR, Calderita G, Arranz R, Fontana J, Granzow H, Risco C. Virus factories: associations of cell organelles for viral replication and morphogenesis. Biol Cell. 2005 Feb;97(2):147-72.
  6. ^ Beate Sodeik, Robert W. Doms, Maria Ericsson, Gerhard Hiller, Carolyn E. Machamer, Wouter van 't Hof, Gerrit van Meer, Bernard Moss, and Gareth Grittiths. Assembly of Vaccinia Virus: Role of the Intermediate Compartment Between the Endoplasmic Reticulum and the Golgi Stacks. The Journal of Cell Biology, Volume 121, Number 3, May 1993 521-541
  7. ^ María L. Salas, Germán Andrés. African swine fever virus morphogenesis. Virus Research 173 (2013) 29– 41
  8. ^ a b Marie Suzan-Monti, Bernard La Scola, Lina Barrassi, Leon Espinosa, Didier Raoult. Ultrastructural Characterization of the Giant Volcano-like Virus Factory of Acanthamoeba polyphaga Mimivirus. PLoS ONE 2(3): e328. doi:10.1371/journal.pone.0000328. 2007
  9. ^ Fernando Tourı́s-Otero, Marcelo Cortez-San Martı́n, José Martı́nez-Costas, Javier Benavente. 374Avian Reovirus Morphogenesis Occurs Within Viral Factories and Begins with the Selective Recruitment of σNS and λA to μNS Inclusions . Journal of Molecular Biology Volume 341, Issue 2, 6 August 2004, Pages 361–374Avian Reovirus Morphogenesis Occurs Within Viral Factories and Begins with the Selective Recruitment of σNS and λA to μNS Inclusions
  10. ^ Fontana J, López-Iglesias C, Tzeng WP, Frey TK, Fernández JJ, Risco C.Virology. Three-dimensional structure of Rubella virus factories. 2010 Sep 30;405(2):579-91. doi: 10.1016/j.virol.2010.06.043. Epub 2010 Jul 23.
  11. ^ Francis Harper, Yves Gaudin and Danielle Blondel Xavier Lahaye, Aurore Vidy, Carole Pomier, Linda Obiang, Transcription and Replication Evidence that NBs Are Sites of Viral (NBs) in Rabies Virus-Infected Cells: Functional Characterization of Negri Bodies. 2009, 83(16):7948. DOI: 10.1128/JVI.00554-09. J. Virol.
  12. ^ M K Karczewski and K Strebel. Cytoskeleton association and virion incorporation of the human immunodeficiency virus type 1 Vif protein. J. Virol. January 1996 vol. 70 no. 1 494-507
  13. ^ a b c Bak A., Gargani D., Macia J-L., Malouvet E., Vernerey M_S., Blanc S. and Drucker,M. Virus factories of Cauliflower mosaic virus are virion reservoirs that engage actively in vector-transmission. 2013 journal of Virology
  14. ^ a b c d e Moshe A. and Gorovits R. Virus-Induced Aggregates in Infected Cells. Viruses 2012, 4, 2218-2232; doi:10.3390/v4102218
  15. ^ Shalla TA, Shepherd RJ, Peterson LJ. Comparative cytology of nine isolates of Cauliflower mosaic virus. 1980.Virology 102:381–388
  16. ^ Wileman T. Aggresomes and autophagy generate sites for viral infection. Science 2006, 312, 875–878.
  17. ^ Kopito R. Aggresomes, inclusion bodies and protein aggregation. Trends Cell Biol. 2000, 10, 524–530.


Dr. Aman Debbarma(agmc)