Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Banana streak disease



Banana streak disease


  • Last modified
  • 27 March 2018
  • Datasheet Type(s)
  • Invasive Species
  • Pest
  • Preferred Scientific Name
  • Banana streak disease
  • Taxonomic Tree
  • Domain: Virus
  •   Unknown: "DNA and RNA reverse transcribing viruses"
  •     Family: Caulimoviridae
  •       Genus: Badnavirus
  •         Species: Banana streak disease

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Chlorotic streak symptoms of BSV in leaf of cultivar Mysore.
TitleSymptoms on leaf
CaptionChlorotic streak symptoms of BSV in leaf of cultivar Mysore.
CopyrightDavid Jones
Chlorotic streak symptoms of BSV in leaf of cultivar Mysore.
Symptoms on leafChlorotic streak symptoms of BSV in leaf of cultivar Mysore.David Jones


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Preferred Scientific Name

  • Banana streak disease

Other Scientific Names

  • banana streak badnavirus
  • Banana streak GF virus
  • Banana streak Mysore virus
  • Banana streak OL virus

International Common Names

  • French: mosaïque en tirets du bananier

English acronym

  • BSMyV

EPPO code

  • BSV000 (Banana streak badnavirus)

Taxonomic Tree

Top of page
  • Domain: Virus
  •     Unknown: "DNA and RNA reverse transcribing viruses"
  •         Family: Caulimoviridae
  •             Genus: Badnavirus
  •                 Species: Banana streak disease

Notes on Taxonomy and Nomenclature

Top of page Banana streak disease (BSD) was for 20 years or so considered to be caused by variable isolates of a single virus, designated Banana streak virus (Lockhart, 1986). However, it has been known for over a decade that some 'isolates' that cause the disease differ biologically, serologically and genomically (e.g., Lockhart and Olszewski, 1993; Geering et al., 2000; Harper et al., 2004). More recently it has been demonstrated that 15 such isolates in Uganda differ sufficiently in genome sequence to justify their recognition as distinct virus species (Harper et al., 2005). The International Committee on Taxonomy of Viruses has so far recognized Banana streak GF virus (BSGFV), Banana streak Mysore virus (BSMyV) and Banana streak OL virus (BSOLV) as distinct viruses (Geering et al., 2005; Hull et al., 2005). This is a complex disease situation; this description, therefore, refers to all the related viruses that induce BSD. All are species of the Badnavirus genus, one of six genera included in the Caulimoviridae family (Hull et al., 2005). The name of the genus is an acronym of BAcilliform DNA VIRUSes.


Top of page Viruses causing banana streak disease (BSD) have non-enveloped, bacilliform particles measuring ca 130-150 x 30 nm and containing a circular dsDNA genome of 7.4 kb (Lockhart, 1986). The particles occur in vivo randomly or in large groups in cytoplasm, but not in inclusion bodies or in membrane-bound structures. A number of serologically and phenotypically distinct, naturally occurring virus isolates that caused BSD were previously identified, and some of these have recently been shown to be similar but distinct viruses and named Banana streak GF virus, Banana streak Mysore virus and Banana streak OL virus (Geering et al., 2005; Hull et al., 2005).


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Banana Streak Disease (BSD) has a very wide geographical distribution; its cause was for long unrecognized as its symptoms were often mistaken for those of Cucumber mosaic virus and the causal viruses were not recognized until the first was purified and characterized by Lockhart (1986). As banana has long been cultivated in all countries in which BSD occurs, and the disease has probably occurred for much longer than 50 years (Wardlaw, 1961), the causal viruses are now probably best considered as native to these countries.

In Taiwan, Su (1997) first reported the disease on cv. Mysore in the greenhouse of the Taiwan Banana Research Institute. The disease had spread in the nearby area and The Bureau of Animal and Plant Health Inspection and Quarantine (BAPHIQ) responded by eradicating infected plants between 1997 and 1999. The disease has not been found in banana plantations in Taiwan since the eradication through a monitoring programme conducted by Dr Su.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


ChinaPresentNative Invasive Diekmann and Putter, 1996; Rao et al., 2005
IndiaPresentNative Invasive Diekmann and Putter, 1996
-KarnatakaPresentCherian et al., 2004
-KeralaPresentCherian et al., 2004
IndonesiaPresentDiekmann and Putter, 1996; Davis et al., 2000; Furuya et al., 2012
JordanWidespreadEPPO, 2014
MalaysiaPresentNative Invasive Diekmann and Putter, 1996
PhilippinesPresentNative Invasive Diekmann and Putter, 1996
Sri LankaPresentNative Invasive Diekmann and Putter, 1996
TaiwanEradicatedSu et al., 1997; EPPO, 2014
ThailandPresentNative Invasive Diekmann and Putter, 1996


BeninPresentNative Invasive Diekmann and Putter, 1996
CameroonPresentNative Invasive Gauhl et al., 1999a; Diekmann and Putter, 1996
Cape VerdePresentNative Invasive Diekmann and Putter, 1996
Côte d'IvoireWidespreadNative Invasive LassoudiFre, 1974; Diekmann and Putter, 1996; EPPO, 2014
EgyptRestricted distributionEPPO, 2014
GhanaPresentNative Invasive Diekmann and Putter, 1996
GuineaPresentNative Invasive Diekmann and Putter, 1996
KenyaPresentNative Invasive Diekmann and Putter, 1996
MadagascarPresentNative Invasive Diekmann and Putter, 1996
MalawiPresentNative Invasive Diekmann and Putter, 1996
MauritiusPresentNative Invasive Diekmann and Putter, 1996
MoroccoWidespreadNative Invasive Diekmann and Putter, 1996; EPPO, 2014
NigeriaPresentNative Invasive Dahal et al., 2000a; Dahal et al., 2000b; Diekmann and Putter, 1996; Agindotan et al., 2003
RwandaWidespreadNative Invasive Diekmann and Putter, 1996; EPPO, 2014
South AfricaPresentNative Invasive Dahal et al., 2000a; Diekmann and Putter, 1996
-Canary IslandsAbsent, unreliable recordDiekmann and Putter, 1996; EPPO, 2014
TanzaniaRestricted distributionNative Invasive Sebasigari and Stover, 1988; Diekmann and Putter, 1996; EPPO, 2014
-ZanzibarRestricted distributionSebasigari and Stover, 1988
UgandaPresentNative Invasive Harper et al., 2002a; Kubiriba et al., 2001a; Diekmann and Putter, 1996; Harper et al., 2004

North America

USAPresentPresent based on regional distribution.
-FloridaPresentDiekmann and Putter, 1996

Central America and Caribbean

Costa RicaPresentNative Invasive Diekmann and Putter, 1996; Pasberg-Gauhl and Lockhart, 2000
CubaPresentNative Invasive Diekmann and Putter, 1996; Hernandez et al., 2002
GrenadaPresentNative Invasive Diekmann and Putter, 1996
GuadeloupePresentNative Invasive Diekmann and Putter, 1996
HaitiPresentNative Invasive Lockhart and Jones, 1999
HondurasPresentNative Invasive Diekmann and Putter, 1996
JamaicaPresentNative Invasive Diekmann and Putter, 1996
NicaraguaPresentNative Invasive Lockhart and Jones, 1999
Puerto RicoPresentNative Invasive Lockhart and Jones, 1999
Saint LuciaPresentNative Invasive Lockhart and Jones, 1999
Trinidad and TobagoPresentNative Invasive Diekmann and Putter, 1996
United States Virgin IslandsPresentNative Invasive Diekmann and Putter, 1996

South America

BrazilPresentNative Invasive Diekmann and Putter, 1996; Brioso et al., 2000
ColombiaPresentNative Invasive Diekmann and Putter, 1996
EcuadorPresentNative Invasive Diekmann and Putter, 1996
VenezuelaPresentNative Invasive Diekmann and Putter, 1996; Garrido et al., 2004; Garrido et al., 2005


PortugalPresentPresent based on regional distribution.
-MadeiraPresentNative Invasive Diekmann and Putter, 1996
SpainAbsent, unreliable recordEPPO, 2014


AustraliaPresentNative Invasive Thomas et al., 1994; Diekmann and Putter, 1996; Geering et al., 2000; Daniells et al., 2001
New CaledoniaPresentNative Invasive Diekmann and Putter, 1996
Papua New GuineaPresentNative Invasive Diekmann and Putter, 1996; Davis et al., 2000
SamoaPresentNative Invasive Thomas et al., 1994; Diekmann and Putter, 1996; EPPO, 2014
TongaPresentThomas et al., 1994; Lockhart and Jones, 1999

Risk of Introduction

Top of page BSV has been found in many banana-producing countries. However, in some, such as Ecuador, it seems to be spreading and causing considerable damage, whereas in others it is rarely seen and then only in one or two cultivars. Differences may be related to the causal virus isolate or vector activity or both. Until more is known about the viruses causing BSD, it would be prudent to prevent movement of the virus between countries in Musa germplasm. Such viruses can be carried in tissue culture without symptoms so extreme care must be taken. Only tissue cultures derived from meristems from quarantined and indexed plants should be permitted to move across borders. Even then, because stresses caused by tissue culturing may initiate episomal virus, care must be taken.

Research is being conducted at the University of Gembloux in Belgium to find methods of eradicating virus from infected banana clones.

Hosts/Species Affected

Top of page Banana cultivars derived from M. acuminata and banana and plantain cultivars derived from crosses between M. acuminata and M. balbisiana are the main hosts of Banana streak viruses (BSV). Isolates of Sugarcane bacilliform virus, which is very closely related serologically to that infecting banana (Lockhart and Autry, 1988), will infect banana and induce symptoms of banana streak, but the virus froim banana has not been successfully transferred from banana to sugarcane (Lockhart, 1995).

Ensete has been infected with BSV (Diekmann and Putter, 1996). A badnavirus causing streak symptoms in Ensete ventricosum (enset) in Ethiopia (Tessera and Quimio, 1999) is also probably a strain of BSV (Lockhart and Jones, 1999).

Growth Stages

Top of page Flowering stage, Fruiting stage, Vegetative growing stage


Top of page Symptom expression varies depending on the isolate of the pathogen, the host cultivar and the environment and can vary from an inconspicuous flecking to lethal necrosis. However, the most common symptoms are narrow, discontinuous and sometimes continuous chlorotic or yellow streaks that run from the leaf midrib to the margin. In some cases, spindle or eye-shaped patterns are present. Yellow blotches have also been associated with banana streak. Symptoms can be sparse or concentrated. Sometimes the lamina can be distorted. Streaks later darken to orange and often become brown or black. Necrosis has also been seen on the midrib and petiole. Necrosis occurs more under low temperature, short-day conditions (Lockhart and Jones, 1999).

A characteristic of infection is the periodicity of symptom expression in leaves. Plants may not show streak symptoms in all leaves and, for several months at a time, emerging leaves may be symptomless or show only slight symptoms. Symptom expression seems to be associated with the change of seasons and fluctuating temperatures may play a role (Dahal et al., 1998a, 2000a,b). The intensity of symptoms has been associated with the concentration of virus in the tissue; the higher the virus concentration, the more severe the symptoms (Dahal et al., 1998b). Plants with BSD may appear symptomless at some stage in their growth cycle as leaves with symptoms are shed and new leaves appear without symptoms due to factors discussed above. Some infected land races show no symptoms even under fluctuating environmental conditions (Dahal et al., 1998a).

Other symptoms associated with BSD are stunting, cigar leaf necrosis, internal necrosis of the pseudostem, a reduction in bunch size, incomplete emergence of bunches and bunches emerging through the side of the pseudostem. Occasionally, dark streak symptoms may be visible on the pseudostem and fingers may be distorted (Lockhart and Jones, 1999).

In Australia, broad yellow lines in the leaf lamina parallel to the midrib, leaf twisting, grooves in the base of the pseudostem and an abnormal arrangement of leaves similar to the traveller's palm (Ravenala madagascariensis) have also been associated with banana streak disease in 'Williams' (AAA, Cavendish subgroup) (Daniells et al., 1998).

Three phases of symptom expression have been recognized in commercial Cavendish plantations in Ecuador. The first is the appearance of chlorotic streaks in leaves, the second is the appearance of dark blotches on the pseudostem and midrib and the third is the splitting of the outer leaf sheaths of the pseudostem sometimes as far up as the petiole. This allows entry of a bacterium that cause a soft rot of the base of the pseudostem. If the plant produces a bunch, peel splitting and necrotic spot and streak symptoms can appear on fruit. Similar symptoms have been seen on 'Grand Nain' (AAA, Cavendish subgroup) in Costa Rica (Lockhart and Jones, 1999).

In the state of Tamil Nadu in India, leaf and aberrant bunch formation symptoms are common on 'Poovan' and seem to increase in severity with the number of crop cycles (DR Jones, Montpellier, France, 1995, personal communication; Thiribhuvanamala and Sabitha Doraisamy, 2001).

List of Symptoms/Signs

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SignLife StagesType
Fruit / abnormal shape
Fruit / discoloration
Fruit / lesions: black or brown
Fruit / reduced size
Leaves / abnormal colours
Leaves / abnormal forms
Leaves / necrotic areas
Stems / dieback
Stems / internal discoloration
Whole plant / dwarfing

Biology and Ecology

Top of page Before it was shown that virus isolates causing BSD were better considered as separate virus species (Geering et al., 2005; Hull et al., 2005), it was known that they differed biologically, serologically and genomically (Lockhart and Olszewski, 1993; Lockhart and Jones, 1999; Geering et al., 2000). The range of isolates or species that induce BSD has in the past created practical problems for reliable detection and diagnosis.

It has been shown that genomic sequences are integrated into the genomic DNA of Musa and Ensete. Virus-related sequences have been found in more than 400 Musa genotypes by PCR amplification (LaFleur et al., 1996; Geering et al., 2001; Harper et al., 2002). While all Musa genotypes appear to contain integrated viral sequences, the nature of these sequences is variable. Of two such integrated sequences that have been characterized, one is incapable of giving rise to episomal BSV infection. There is good evidence, however, that a second integrated sequence is the source of de novo episomal BSV infection in banana including a significant number of tetraploid hybrids which have been bred for improved yield and disease resistance. The development of episomal infection from integrated viral sequences is linked to in vitro propagation and possibly other stress factors (Krikorian et al., 1999; Ndowora et al., 1999).

Expressible virus integrants have been found in Musa balbisiana and some AAB, ABB and AAAB clones. However, they were not been found in AA or AAA clones tested indicating that de novo synthesis may only occur in cultivars/bred hybrids with the B genome (BEL Lockhart, Minnesota, USA, 1999, personal communication). A distinct virus or strain which was first isolated and characterized from an IITA plantain hybrid ('TMPx 4698') bred in Nigeria (Harper and Hull, 1998), is believed to be the product of these expressible virus integrants (BEL Lockhart, Minnesota, USA, 1999, personal communication).

Means of Movement and Dispersal

Top of page Transmission

Attempts to transmit the causal viruses by mechanical inoculation using abrasives have been unsuccessful. The virus, therefore, is unlikely to be transmitted on cutting tools or during cultural operations. It is also not soil-borne (Lockhart and Jones, 1999).

However, like some other badnaviruses, those causing BSD are transmitted from infected to healthy plants by mealybugs (Hemiptera; Pseudococcidae). The virus is transmitted in a semi-persistent manner from banana to banana by the citrus mealybug (Planococcus citri) and an unidentified Pseudococcus sp. (Lockhart and Jones, 1999), and, in screenhouse experiments, by the pineapple mealybug (Dysmicoccus brevipes) and the pink sugarcane mealybug (Saccharicoccus sacchari) (Kubiriba et al., 2001 a,b). The virus does not multiply in the insect vectors and is not transmitted transovarially. Banana and plantain are hosts of a range of mealybug species (Watson and Kubiriba, 2005). Although all possible vectors have not yet been determined, 20 species and 14 genera of mealybugs infest banana and plantain in Africa and probably elsewhere (Watson and Kubiriba, 2005); it is possible that other mealybug species, such as Planococcus musae in Nigeria and Pseudococcus comstocki in Ecuador may also be vectors. The pink sugarcane mealybug, S. sacchari, transmits Sugarcane bacilliform virus from sugarcane to banana (Lockhart and Autry, 1991). In many tropical areas, such as Tamil Nadu in India, sugarcane is grown in close proximity to banana and transmission from the former to the latter may occasionally occur in nature. The pattern of field spread of BSD in Uganda has been reported by Kuririba et al. (2001b).

Observations in many countries suggest that the spread of the causal virus from plant to plant by mealybug vectors may be limited in occurrence. However, mealybugs are common on banana in some locations, such as in Ecuador where the high incidence of infection in commercial plantations may be a result of vector dissemination (Lockhart and Jones, 1999).

Seedborne spread

Studies in Australia with Banana streak Mysore virus have shown that the virus is seedborne (Daniells et al., 1995). Other viruses that induce BSD may also be so transmitted.

Long distance dissemination

The principal means of long-distance dissemination is in vegetative planting material, such as suckers or tissue cultures. Viruses inducing BSD cause systemic infection. All tissue cultures derived from meristems excised from diseased plants have been found to carry BSV (Lockhart and Jones, 1999).

Seedborne Aspects

Top of page Pathogen Transmission

Studies in Australia with Banana streak Mysore virus (BSMyV) have shown that the virus is seedborne (Daniells et al., 1995). Interestingly, leaf striping in plants of the subgroup Mysore was originally thought to be a genetic trait because the symptom was transferred to progeny in breeding experiments in Trinidad (Wardlaw, 1961). However, it is now known that many clones in the Mysore subgroup are infected with BSMyV because stripe symptoms typical of the virus are often seen in this cultivar. Therefore, the most logical explanation for the above report is that the virus was carried through seed to the progeny.

Vectors and Intermediate Hosts

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Planococcus citriInsect


Top of page In Côte d'Ivoire, yield losses in 'Poyo' (AAA, Cavendish subgroup) over two cycles varied between 7% on plants with mild BSD symptoms to 90% on plants with severe symptoms (Lassoudière, 1974). The intensity of symptoms may be related to virus concentrations in plants; if concentrations are high at the time of flowering and fruit filling, yield losses can be expected to be high (BEL Lockhart, Minneapolis, USA, 1994, personal communication).

In Nigeria and Rwanda, internal necrosis results in plant death. BSD symptoms have been seen on plants in just over half the villages surveyed in southern Nigeria and southern Cameroon with incidence ranging from 0.5 to 17% (Gauhl et al., 1999a, b).

In India, yield losses from infected 'Poovan' (AAB, syn. 'Mysore') are thought to be very high in the third crop cycle when bunches can 'choke' on emergence or emerge through the side of the pseudostem. As a consequence, 'Poovan' plantations need to be replanted every 3 years.

In plantations of Cavendish cultivars in Costa Rica and Ecuador, BSD results in severe symptoms on fruit, which makes them unmarketable. In addition, the virus causes the pseudostem to split resulting in a bacterial infection that eventually kills the plant. Drastic methods, which can include the destruction of all plants in a 50 m², are sometimes taken in an effort to control the disease in export plantations in Ecuador (Lockhart and Jones, 1999).

Actual yield losses in some banana and plantain cultvars will be difficult to assess because clones seem to be universally affected. Symptoms of BSD can be seen at some time on almost all 'Mysore' and 'Cuerno' (AAB, Plantain subgroup) plants. Most accessions of plantain in the in vitro germplasm collection at the INIBAP Transit Centre at Leuven, Belgium, have indexed positive for a virus causing BSD (I Van den Houwe, Leuven, Belgium, 1999, personal communication). This may reflect the widespread occurrence of BSV in plantain cultivars. In Australia, infection can result in an 18 day delay in harvest and a 6% loss of yield annually (Daniells et al., 2001).


Top of page The detection of BSD by symptoms alone is unreliable as symptomless infections can occur (Dahal et al., 1998, 2000a,b) and any of several viruses may be involved (see Notes on Taxonomy and Nomenclature). Tests need to be undertaken to determine if plants are infected and to identify the causal virus.

The ability of several viruses to cause BSD, has posed the most serious obstacle to the reliable detection of the virus in infected tissue. Serological heterogeneity has made it difficult to develop routine virus indexing protocols capable of detecting the complete range of virus isolates (Lockhart and Olszewski, 1993). A significant improvement in detection by ELISA was achieved by developing assay protocols using polyclonal antibodies produced in two different animal species (Ndowora, 1998), or using monoclonal antibodies in assays (Agindotan et al., 2003). In spite of marked improvements in the reliability of virus detection by ELISA, there remain isolates or viruses that are detected weakly or not at all if heterologous antisera are used. However, these and all other strains or viruses can be detected by immunosorbent electron microscopy (ISEM) using partially purified leaf-tissue extracts (Bouhida et al., 1993; Ndowora and Lockhart, 2000; Garrido et al., 2005). Unfortunately, this is expensive and laborious and requires specialised equipment and skills (Lockhart and Jones, 1999).

Genome-based methods of virus detection (EG nucleic acid hybridization, PCR amplification), which are potentially highly sensitive, are seriously compromised by both genomic heterogeneity among viruses inducing BSD and the occurrence of integrated virus sequences in the Musa genome (LaFleur et al., 1996; Ndowora et al., 1999). However, the use of IC-PCR (Thottapilly et al., 1997; Harper et al., 1999, 2002b; Cherian et al., 2004; Garrido et al., 2005; Rao et al., 2005) avoids false positives due to integrated viral sequences and is a potential tool in diagnosing infection.

Detection and Inspection

Top of page If possible, plants should be grown under cool or fluctuating temperatures. The leaves should be inspected for chlorotic or necrotic streak or fleck symptoms. Not all leaves may show symptoms; often streaks are only seen on one or two leaves on an infected plant. Incomplete bunch emergence or bunches emerging through the pseudostem also suggest that the plant may be virus infected.

Plants may be symptomless (see Symptoms) and tests need to be undertaken to determine if the virus is present or absent (see Diagnostic Methods).

Similarities to Other Species/Conditions

Top of page Chlorotic and yellow streak symptoms of BSD can easily be mistaken for those induced by Cucumber mosaic virus (CMV). However, whereas CMV symptoms occur on the leaf midrib, this is not the case with BSV. Discontinuous or continuous necrotic streaks in leaves, where found, usually indicate that the disease is caused by a BSV, although some strains of CMV can also cause leaf necrosis. Internal necrosis of the pseudostem can be caused by a BSV or by severe strains of CMV.

Many isolates of BSV and Sugarcane bacilliform virus are serologically related (Lockhart and Olszewski, 1993).

Prevention and Control

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Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.

Infected plants should be destroyed and replaced with virus-tested plants. Although such plants are usually obtained by meristem tip culture (e.g., Helliot et al., 2001; Hernandez et al., 2002; Rao et al., 2005), they are also obtainable by using cryopreservation (Helliot et al., 2002) or by treating micro-plants with acyclic nucleoside phosphonate analogues such as adefovir or tenovir (Helliot et al., 2003a). Only tissue cultures derived from meristems from virus-tested plants should move internationally and be mass multiplied. Even then, care must be taken because of the possible de novo synthesis of the virus in tissue culture.

Mealybug vectors should be controlled if virus incidence is high and the disease appears to be spreading from plant to plant. The virus is unlikely to be spread on cutting tools or by mechanical means.

In Ecuador, where banana streak is a serious problem in some commercial Cavendish plantations, plants with symptoms are quickly destroyed after spraying with insecticide in an effort to contain the outbreak. If 10 plants with symptoms are seen in a 50 m² area, then all plants in that area are destroyed. However, these practices have failed to stop spread and more drastic action is being considered (Lockhart and Jones, 1999).


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