MicrobiologyBytes: Virology: Iridoviruses Updated: January 28, 2007 Search


Introduction | Taxonomy | Morphology | Genome | Replication | Gene expression | Pathogenesis


The family Iridoviridae contains a diverse array of large icosahedral viruses that replicate in the cytoplasm of infected cells. The word Iridoviridae is derived from Iris who was the Greek goddess of the rainbow. This is due to the "rainbow like" iridescence observed in heavily infected insects and pelleted samples of invertebrate iridoviruses.

Iridovirus-infected grub

Larvae of the grass grub Costelytra zealandica displaying blue colouration of the hindgut due to iridovirus infection.

Purified Tipula iridescent virus

Pellet of purified Tipula iridescent virus

This iridescence facilitated the first detection of an iridovirus when Claude Rivers, in March of 1954, discovered crane fly larvae (Tipula spp) glowing with patches of blue colouration. Iridoviruses have since been isolated from both invertebrate and non-mammalian vertebrate hosts. A common feature of most of these hosts is the aquatic or moist environment in which they are found. Iridoviruses have received attention because of the problems they pose to aquacultural practices and because of their potential use in the biological control of insect pests.

Paracrystalline array of virus particles

Paracrystalline array of virus particles within infected cell. This array gives rise to the iridescent phenomenon.

Sf21 tissue culture cell

Sf21 tissue culture cell showing cytoplasmic localisation of assembling Wiseana iridescent virus particles. N= nucleus, VC = viroplasmic centre


The family Iridoviridae is comprised of four genera, two infecting vertebrates and two infecting invertebrates.


Vernacular name

Host species

Type species


Small iridescent insect virus

Invertebrates (mainly insects)

Chilo iridescent virus (IV6)


Large iridescent insect viruses


Mosquito iridescent virus (IV3)


Lymphocystis disease virus


Lymphocystivirus type 1 (LCDV-1)


Frog virus


Frog Virus 3 (FV3)

The current ICTV list of recognised Iridoviridae members contains much redundant data. The wide host range displayed by members of this family has resulted in isolates of a single virus species being described and named more than once because of their isolation from different hosts. The host of isolation also confuses taxonomy within the family with recently identified fish iridoviruses seemingly more related to ranaviruses than to lymphocystiviruses. The pitfalls in iridovirus taxonomy are only just beginning to be addressed using molecular techniques.


Representation of the homologies between invertebrate iridovirus major capsid genes highlighting the region used for phylogenetic analysis. Bars represent the major capsid proteins from each virus with greyscales ranging from black for 100% homology to the CzIV protein to white for 0% homology.

For example, the PCR amplification and sequencing of a 500 bp fragment of the major capsid protein gene from a number of invertebrate iridoviruses suggests the genus Iridovirus can be further divided into three groups.

Phylogenetic tree of Iridoviruses

Phylogenetic tree of the genus Iridovirus based on partial MCP sequence

Iridovirus origins

Countries of virus isolation




Country of isolation



crane fly




scareb grub




rice stem borer




porina caterpillar

New Zealand

CzIV (IV16)


grass grub

New Zealand



black fly


BbIV (IV23)


black beetle

South Africa

IV24 (AIV)


honey bee




meal worm




corn earworm








Velvetbean caterpillar




Japanese beetle





World wide


Electron micrograph of an iridovirus

Electron micrograph of a typical iridovirus

Iridoviruses are large (120 to 300 nm in diameter) non-occluded viruses with icosahedral symmetry. An iridovirus virion is composed of three concentric domains; an outer proteinaceous capsid, an intermediate lipid membrane with associated polypeptides, and a central core containing DNA-protein complexes. Some, but not all, viruses possess an outer envelope acquired by budding through host membranes. Fibrillar structures have also been observed protruding from capsid subunits of LCDV-1, MIV, and CIV, but not from FV3. Depending on the detection method used iridoviruses possess between 25 to 75 structural proteins ranging in molecular weight from 12,000 to 150,000 kDa. A common feature of all iridoviruses is the presence of a major capsid protein of around 50 kDa that accounts for up to 45% of total virion protein.

Prolonged storage of Sericesthis iridescent virus (SIV) in distilled water at 4°C led to the disintegration of virions into triangular, pentagonal and linear fragments consisting of 55, 16, and 9 subunits respectively. These observations led Wrigley to propose the following 1562 morphological subunit structure for SIV. Later studies on TIV suggested that a structure represented by 1472 subunits may be more appropriate. Larger iridoviruses break down into larger but morphologically similar subunits.

Iridovirus structure

Schematic diagram adapted from N.G. Wrigley 1969 (J. Gen. Virol. 5:123-134)


Iridoviruses contain a single copy linear dsDNA genome that ranges in size from 150 to 280 kbp depending on viral species. The genomes appear unique within the eucaryotic viruses in that they are terminally redundant and cyclically permuted. This structure is a result of the resolution of genome concatamers during DNA replication (see replication).

Iridovirus genome

A simplistic view of terminal redundancy and cyclic permutation.

During replication multiple copies of a hypothetical viral genome consisting of 10 genes (A) forms a long concatamer (B). The resolution of this concatamer (C) results in packaged DNA lengths that contain a complete genome as well as duplicated copies of some genes (terminal redundancy). The ends of each of these packaged DNAs differs from one virus particle to the next (cyclic permutation).

This genomic structure has been found in all iridoviruses so far studied. Subtle variations do occur between different genera in the cyclic permutation. The packaged DNA ends within a population of FV3 are confined to regions representing 25% of the genome whereas in CIV and LCDV-1 the permutation is completely random covering 100%. Plasmid rescue experiments identified six origins of replication in CIV, a feature consistent with cyclic permutation. Three of these origins have been sequenced and all were predicted to form hairpin structures.

The particles of Tipula iridescent virus (TIV) appear unique in that they contain at least two genomic fragments, one of genome length and another of approximately 11 kbp. This smaller subgenomic fragment hybridises to defined regions of the genome but it is not known whether it also contains unique sequences or what its role is.


The replication of iridoviruses comes mainly from studies of FV3 and this has become the model for iridovirus replication. Although packaging occurs in the cytoplasm of infected cells, a nuclear stage is also present.

Iridovirus replication

FV3 replication model adapted from R. Goorha 1982 (J. Virol. 43(2):519-528)

1) Virus particles enter the cell by pinocytosis and uncoating occurs.

2) Viral DNA is transported to the cell nucleus where host macromolecular synthesis is rapidly shutdown. Transcription is initiated by virally modified host RNA polymerase II.

3) Parental DNA is used to produce genome and greater than genome length DNA. This becomes the template for cytoplasmic replication.

4) Progeny DNA is transported into the cytoplasm where large concatamers of viral DNA are formed by recombination. Transcription of very late transcripts may also take place in the cytoplasm.

5) Concatamers are resolved into packaged lengths, possibly by a headful packaging approach. Virions exit the cell by budding or cell lysis.

Genome replication

Possible recombination dependent iridovirus replication.

Origin dependent replication results in the production of duplex DNA with single stranded 3' ends (A). These single stranded regions are capable of recombination within the same duplex (C) or with another DNA molecule (B). In this this way these 3' ends serve as primers for further DNA replication. The result is a large interlinked and replicating DNA concatamer. Modified from G. Mosig 1987 (Ann. Rev. Genet. 21:347-371)

Gene expression

Studies of both vertebrate and invertebrate iridoviruses show transcription occurs in a temporal manner with three stages; immediate-early, delayed-early, and late. There is both positive induction and some negative feedback on transcription at each level by translational products of other temporal stages.

Gene expression

Frog virus 3 transcription control model


Little is known about the pathogenesis of iridoviruses. The pathogenesis is, however, temperature dependent and iridoviruses are thus confined to poikilothermic hosts. Iridoviruses from the blackfly, Simulium spp., are found in two states, covert (inapparent) and patent (lethal), the ratios of each dependent on environmental conditions and host densities. In a lethal infection by insect iridoviruses the fat bodies and haemocytes are the initial sites of replication, this leading to a systemic infection. Insects become flaccid and iridescent 7-10 days post-infection although death may take 3 weeks or longer.

FV3 is not known to cause disease in naturally occurring frog populations although frog embryos and larvae die within 15 days if inoculated with virus. FV3 can cause edema of tadpole tails but has no apparent effect if inoculated into adult frogs.

LCDV-1 causes a nonlethal viral disease of many marine and freshwater fish. A characteristic of the disease is the presence of enormously enlarged host cells (cells can increase in volume by a factor of 106). Infected fish often have nonmalignant tumour-like growths and raspberry-like lesions associated with their skin.

Although FV3 and LCDV-1 appear to be non-lethal, high mortality rates amongst various frog and fish populations have been caused by other viruses of the Iridoviridae family.

Introduction | Taxonomy | Morphology | Genome | Replication | Gene expression | Pathogenesis

© Webby, Watson & Kalmakoff
University of Otago, Dunedin, New Zealand
, 1998.