A brief presentation on Chikungunya

Dr Saif Ullah Munshi
Chikungunya Virus (CHIKV) is a virus that is transmitted from human to human mainly by infected Aedes albopictus and Aedes aegypti mosquitoes

CHIKV infection
It is more urban localities
Usual age group is above 15 years
Less common in children and infants
Family clustering of cases usual
Attack rates vary from 3 to 40% of population
Average attack rate is 10%
Herd immunity restricts further spread
Symptoms typically occur in 72–97% of those infected
In endemic area, only 18% of infections resulted in clinical
illness, possibly due to re-exposure
Post CHIKV Arthralgia / Arthritis
When it was started ?
  First published report is from Africa in1955 by Marion Robinson  & W.H.R. Lumsden
Major epidemics appear cyclically
Recent outbreak in the Indian Ocean after 20 years of dormancy
Chikungunya: Global distribution

Most Recent Epidemics
1963 to 1965 - An epidemic was reported in Calcutta
1999- Epidemic of CHIKV occurred in Malaysia
2005- French island of Réunion in the Indian Ocean, Mauritius, Madagascar and Seychelles
Hong Kong and Malaysia- early 2006
Seroprevalence Chikungunya in major cities of Bangladesh  
Transmission
Reservoir – Non-human primates in Africa
No animal reservoir is found in India
Maintained in nature by man – mosquito – man cycle
Vector – Aedes aegypti, Ae. albapticus mosquito
Same vector as for Dengue and Yellow fevers
Vehicle of transmission – None
Transmit through mosquito bite, vertical transmission may occur
Incubation Period – 2 days to 12 days

Vertical Transmission
Mother to fetus transmission can occur
Reported between 3 to 4.5 months of gestation
Maternal IgG develops in 2 weeks after CHIKV
This passes through placenta – confers protection
Intra-partum risk is 48% if mother has viremia
Neonatal infections are very mild; fully recover
No miscarriages or congenital malformations

How & where it effects ?
Which cells CHIKV infects?
Human epithelial and endothelial cells, primary fibroblasts, and monocyte-derived macrophages are susceptible to chikungunya virus infection,
Activated B and T CD4+ lymphocytes, monocytes, and monocyte-derived dendritic cells were refractory to chikungunya virus infection
Mechanisms of CHIKV persistence and tissue  inflammation in patients with chronic disease.

(1) Months after the acute infection, monocytes, T cells, and natural killer (NK) cells are still attracted to the inflamed joint, where they become activated.

(2) The infection of macrophages in joints is associated with local inflammation and the production of cytokines, chemokines, and pro-inflammatory effectors, such as MCP-1/CCL-2, IL-8, IL-6, IFN-a, and MMP2 (Matrix Metallopeptidase 2).

(3) The phagocytosis of apoptotic bodies from infected cells probably contributes to viral persistence. Nevertheless, the beneficial or deleterious effect of local inflammation on viral persistence remains unclear.

(4) When it occurs, arthritis is accompanied by high rates of fibroblast apoptosis and cartilage destruction. Chronic inflammation probably plays a major role in this damage and associated pain.

(5) The potential relationship between local inflammation of the joint and a state of systemic activation, as demonstrated by the presence of inflammation markers in plasma and blood cells, remains unclear. doi:10.1371/journal.pntd.0001446.g002.

The writer is a Professor
Department of Virology,
Bangabandhu Sheikh Mujib
Medical University (BSMMU)

A brief presentation on Chikungunya

Dr Saif Ullah Munshi Chikungunya Virus (CHIKV) is a virus that is transmitted from human to human mainly by infected Aedes albopictus and Aedes aegypti mosquitoes CHIKV infection It is more urban localities Usual age group is above 15 years Less common in children and infants Family clustering of cases usual Attack rates vary from 3 to 40% of population Average attack rate is 10% Herd immunity restricts further spread Symptoms typically occur in 7297% of those infected In endemic area, only 18% of infections resulted in clinical illness, possibly due to re-exposure Post CHIKV Arthralgia / Arthritis When it was started ? First published report is from Africa in1955 by Marion Robinson W.H.R. Lumsden Major epidemics appear cyclically Recent outbreak in the Indian Ocean after 20 years of dormancy Chikungunya: Global distribution Most Recent Epidemics 1963 to 1965 - An epidemic was reported in Calcutta 1999- Epidemic of CHIKV occurred in Malaysia 2005- French island of Runion in the Indian Ocean, Mauritius, Madagascar and Seychelles Hong Kong and Malaysia- early 2006 Seroprevalence Chikungunya in major cities of Bangladesh Transmission Reservoir Non-human primates in Africa No animal reservoir is found in India Maintained in nature by man mosquito man cycle Vector Aedes aegypti, Ae. albapticus mosquito Same vector as for Dengue and Yellow fevers Vehicle of transmission None Transmit through mosquito bite, vertical transmission may occur Incubation Period 2 days to 12 days Vertical Transmission Mother to fetus transmission can occur Reported between 3 to 4.5 months of gestation Maternal IgG develops in 2 weeks after CHIKV This passes through placenta confers protection Intra-partum risk is 48% if mother has viremia Neonatal infections are very mild; fully recover No miscarriages or congenital malformations How where it effects ? Which cells CHIKV infects? Human epithelial and endothelial cells, primary fibroblasts, and monocyte-derived macrophages are susceptible to chikungunya virus infection, Activated B and T CD4+ lymphocytes, monocytes, and monocyte-derived dendritic cells were refractory to chikungunya virus infection Mechanisms of CHIKV persistence and tissue inflammation in patients with chronic disease. (1) Months after the acute infection, monocytes, T cells, and natural killer (NK) cells are still attracted to the inflamed joint, where they become activated. (2) The infection of macrophages in joints is associated with local inflammation and the production of cytokines, chemokines, and pro-inflammatory effectors, such as MCP-1/CCL-2, IL-8, IL-6, IFN-a, and MMP2 (Matrix Metallopeptidase 2). (3) The phagocytosis of apoptotic bodies from infected cells probably contributes to viral persistence. Nevertheless, the beneficial or deleterious effect of local inflammation on viral persistence remains unclear. (4) When it occurs, arthritis is accompanied by high rates of fibroblast apoptosis and cartilage destruction. Chronic inflammation probably plays a major role in this damage and associated pain. (5) The potential relationship between local inflammation of the joint and a state of systemic activation, as demonstrated by the presence of inflammation markers in plasma and blood cells, remains unclear. doi:10.1371/journal.pntd.0001446.g002. The writer is a Professor Department of Virology, Bangabandhu Sheikh Mujib Medical University (BSMMU)