African cassava mosaic virus
(African cassava mosaic)

Preferred Common Name

• African cassava mosaic

Other Scientific Names

• Cassava African mosaic bigeminivirus

International Common Names

• English: cassava latent virus; cassava mosaic
• Spanish: mosaico africano de la yuca
• French: mosaïque africaine du manioc

Local Common Names

• Germany: Cassava Mosaikvirus

English acronym

• ACMV

EPPO code

• ACMV00 (African cassava mosaic begomovirus)

• Domain: Virus
•     Group: "ssDNA viruses"
•         Group: "DNA viruses"
•             Family: Geminiviridae
•                 Genus: Begomovirus
•                     Species: African cassava mosaic virus

African cassava mosaic virus (ACMV) is a member of the genus Begomovirus in the family Geminiviridae. ACMV was the first of 10 recognized and one tentative begomovirus species characterized from cassava plants affected by cassava mosaic disease (CMD). Historically, the first report of CMD came from the Usambaras Mountains range in northeast Tanzania in 1894. The disease was named as ‘Kräuselkrankheit’, a German word that translates to ‘rippling/crinkling illness’ (Warbug, 1894) which describes symptoms observed on affected plants. Although a virus was originally suggested to be the causal agent of CMD (Zimmermann, 1906) and its transmission by Bemisia spp. whiteflies demonstrated (Chant, 1958), it was not until the 1970s when small, quasi-isometric, geminate particles were found in leaf tissue samples from symptomatic CMD-affected cassava (Harrison et al., 1977). The virus was momentarily named as cassava latent virus (CLV) because its sap inoculation into Nicotiana clevelandii did not produce symptoms in this herbaceous host (Bock et al., 1978). Following the molecular characterization of CLV (Stanley and Gay, 1983), the virus was successful sap-inoculated onto N. benthamiana and cassava and typical CMD symptoms produced (Bock and Woods, 1983) thus fulfilling Koch’s postulates and prompting a name change from CLV to ACMV. Fifteen years later, an infectious clone of ACMV was developed and its infectivity onto cassava via biolistic inoculation achieved (Briddon et al., 1998). Over the course of several decades, nine additional viruses and one tentative species have been characterized from CMD-affected cassava worldwide. They are: East African cassava mosaic virus (EACMV; Hong et al., 1993), East African cassava mosaic Malawi virus (EACMMV; Zhou et al., 1998), South African cassava mosaic virus (SACMV; Berrie et al., 1998), East African cassava mosaic Cameroon virus (EACMCV; Fondong et al., 2000), Indian cassava mosaic virus (ICMV; Mathew and Muniyappa, 1992; Saunders et al., 2002), Sri Lankan cassava mosaic virus (SLCMV; Saunders et al., 2002), East African cassava mosaic Zanzibar virus (EACMZV; Maruthi et al., 2004), East African cassava mosaic Kenya virus (EACMKV; Bull et al., 2006) and Cassava mosaic Madagascar virus (CMMGV; Harimalala et al., 2012). A recombinant virus, African cassava mosaic Burkina Faso virus (ACMBFV; Tiendrébéogo et al., 2012) was also characterized from disease-affected cassava but is yet to be recognized as a bona fide species by the International Committee on Taxonomy of Viruses (ICTV). Besides ICMV and SLCMV, all other CMD-associated viruses are of African origin. All CMD-associated viruses are collectively called cassava mosaic geminiviruses (CMGs) or cassava mosaic begomoviruses (CMBs).

The first elucidation of ACMV was achieved when electron micrographs obtained from sap extracts from symptomatic cassava leaves revealed twinned (geminate), small, quasi-isometric particles measuring 15-20 nm in diameter (Harrison et al., 1977; Böttcher et al., 2004). The particle size measures 20 x 30 nm and comprises a 30 kDa coat protein (Stanley et al., 2005). The coat protein encapsidates the bipartite, circular ssDNA DNA A and DNA B genome components of ACMV that are each ~2.7 Kb.

Both genome components are needed for efficient transmission of ACMV and its establishment in otherwise healthy cassava plants (Liu et al., 1997). Once the vector has acquired the virus, a 6-8 hour latent period must elapse before the vector can transmit the virus over an inoculation access period of 20-30 minutes (Dubern, 1994). After acquiring the virus, viruliferous whiteflies remain infective for 9 days but progenies of infective whiteflies do not retain the virus (Dubern, 1994). Thus ACMV is transstadially, but not transovarially, transmitted (Dubern, 1994). Compared with the Asian Bemisia tabaci, the African B. tabaci is more efficient in transmitting CMGs from Africa than those from Asia suggesting a phenomenon of virus-vector-co-adaptation within the cassava pathosystem (Maruthi et al., 2002). Apart from B. tabaci, other whitefly species such as Bemisia afer are known to transmit ACMV (Palaniswami et al., 1996) albeit at a lower efficiency.

ACMV is thought to be native to the African continent and its islands. Although the primary host, cassava, was introduced to Africa from South America in the sixteenth and eighteenth centuries, ACMV has not been reported in the Americas but its disease symptoms were first reported in Tanzania in the nineteenth century (Warbug, 1894) and the causal pathogen studied (Storey, 1936; Storey and Nichols, 1938; Bock and Woods, 1983). In mainland Africa, ACMV occurs in virtually all cassava-growing regions spanning East Africa (Legg, 1999; Ndunguru et al., 2005, 2016; Bull et al., 2006), West and Central Africa (Fauquet and Fargette, 1990; Fondong et al. 2000; Ogbe et al., 2003, 2006; Alabi, 2009) and Southern Africa (Mabasa, 2007; Cossa, 2011; Chikoti et al., 2013; Mulenga et al., 2016). In the 1930s, ACMV symptoms on cassava plants were noticed in Madagascar (Cours et al., 1997) and its distribution alongside other CMGs mapped (Harimalala et al., 2015). Several reports of ACMV in Seychelles, Zanzibar and other islands exist (Fauquet and Fargette, 1990; Thresh and Cooter, 2005). ACMV has a relatively stable genome with fewer species than EACMV-type CMGs but recently a tentative ACMV-like recombinant begomovirus, African cassava mosaic Burkina Faso virus (ACMBFV) was characterized in Burkina Faso (Tiendrébéogo et al., 2012) indicating plasticity of the ACMV genome.

CMGs cause a variety of foliar symptoms on cassava but no pattern is ascribed to any one single virus. Generally, symptoms include yellow or green mosaic, mottling, and misshapen and twisted leaflets (Thottappilly et al., 2003; Alabi et al., 2011). The display of the symptoms may vary in distribution in the fields, from plant to plant and even on the same plant. The pattern of foliar symptoms is influenced by the associated virus species, the presence of sequences enhancing geminivirus symptoms (SEGS) (Ndunguru et al., 2016) and the presence of single or mixed infections, age of the plant, variety responses to infection and environmental factors (Legg and Thresh, 2000; Maruthi et al., 2002; Ogbe et al., 2003). Studies have shown that severe symptoms are usually characteristic of plants infected by mixtures of CMGs, their recombinant variants and/or SEGS. This was evident in plants infected by ACMV/ East African cassava mosaic Uganda variant (EACMV-UG) first recorded in Uganda in the 1990s (Zhou et al., 1998). EACMV-UG is a recombinant virus that arose from recombination of portions of the genomes of ACMV and EACMV (Zhou et al., 1997). The time to symptom expression in an infected plant depend on the mode of infection. Planting material sourced from infected stock display ACMV symptoms in the first few emerging leaves (cutting-borne infection) whereas ACMV infections facilitated by whiteflies (vector-borne infection) require a lag period before the virus titre can build up to levels capable of eliciting symptoms.

Field diagnosis of CMD symptoms may be confusing especially if the fields are also infested with cassava green mites (CGMs); with symptoms looking more severe than normal. Although CMGs affect cassava plants to varying levels of severity, the symptoms produced cannot easily be ascribed to any one virus species by visual inspection of diseased leaves. This is because the mosaic symptoms do not form characteristic patterns associated with specific viruses. In infection complexes, therefore, it is important to confirm the causal species through PCR and ELISA methods.

Vector transmission (biotic)

Vector transmission is the most important and efficient means of within field transmission of ACMV from infected plants to healthy ones. The virus is transmitted in a non-persistent manner and transmission can be optimal with as few as 10 viruliferous whiteflies (Dubern, 1994). Vector mobility is key in ACMV transmission over short (within field) and long (between fields) distances and is aided by wind direction (Fargette et al., 1990).

Accidental introduction

This is not known to be a factor in introduction of ACMV to virus-free areas.

Intentional introduction

There is no information on the intentional introduction of ACMV to new areas, but the literature indicates that most farmers are unfamiliar with the viral aetiology of symptomatic plants, with the consequence that they are oblivious to the presence of the disease in the selection of commonly shared or traded planting materials (Alabi et al., 2015). This is arguably the most important route of movement of ACMV and other CMGs across regions.

The economic impact of ACMV as a single virus is not clearly stated in the literature. However, collectively CMGs have been shown to cause varying levels of yield loss depending on whether they occur as single or mixed infections and the susceptibility of varieties infected (Owor et al., 2004). Because of the difficulty of measuring yield loss attributed only to ACMV or to CMGs, the majority of yield loss estimates were conducted in the twentieth century (Thresh et al., 1994; Thottappilly et al., 2003; Legg et al., 2004). At the time, annual yield loss estimates were approximated at 15% and 24% translating to 12-23 million tonnes or US$ 1.2-2.3 billion (Thresh et al., 1997). In other studies, yield loss estimates were revised upwards to 30% in a region-wide assessment of sub-Saharan Africa (Legg and Thresh, 2000; Legg et al., 2006).

CMD-related yield loss not only impacts crop performance but disrupts the livelihoods of people that depend on cassava as a staple. This was evident in East Africa when a regional pandemic of an unusually severe form of CMD began in Uganda in the early to mid-1990s (Gibson et al., 1996; Otim-Nape et al., 1997) and spread across the East African region causing severe crop loss. The East African CMD pandemic resulted in famine-related deaths (Otim-Nape et al., 1998) reminiscent of the infamous potato late blight disease outbreak in Ireland in the nineteenth century (Alabi et al., 2015).

• Invasive in its native range
• Proved invasive outside its native range
• Has a broad native range
• Abundant in its native range
• Highly adaptable to different environments
• Is a habitat generalist
• Tolerant of shade
• Has high genetic variability

• Altered trophic level
• Host damage
• Increases vulnerability to invasions
• Negatively impacts agriculture
• Negatively impacts livelihoods
• Negatively impacts trade/international relations

• Rooting

• Highly likely to be transported internationally accidentally
• Highly likely to be transported internationally illegally
• Difficult/costly to control