Preventing the spread of HTLVs

Human T-cell lymphotropic virus I (HTLV-I) was the first human pathogenic retrovirus to be isolated. It is an ancient virus that appears to have migrated with infected human populations for perhaps thousands of years. As 95% of people infected with HTLV-I never develop symptoms¹, blood screening for antibodies is necessary for the proof of infection required to prevent further transmission. Here we take a closer look at HTLV.

In patients infected with HTLV, the body's immune system detects and tries to remove the virus. Unable to clear it completely, a balance is reached where viral reproduction continues but is controlled by the immune system. The patient can remain well but in a state of asymptomatic carriage. Carriers are more open to opportunistic infections caused by alterations to the host's immune function rather than the virus itself and, in a few cases, symptoms do develop.

HTLV-I is a lifelong infection that can cause T-cell leukaemia and T-cell lymphoma in adults. It has also been associated with certain demyelinating diseases, referred to as HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP), in which the myelin sheath of neurons is damaged. HAM/TSP is a slowly progressive disorder primarily affecting the lower limbs, leading to stiffness and weakness of the legs, backache, a ‘weak’ bladder and constipation.

First discovered in 1979 in the laboratory of Robert C. Gallo at the National Cancer Institute by Bernard Poiesz and Francis Ruscetti and their co-workers, HTLV is a single-stranded RNA retrovirus belonging to the family of Retroviridae (genus: Deltaretrovirus). HTLV-I infects approximately 15 to 20 million people worldwide².

Shortly after the discovery of HTLV-I, a second, closely related virus was found and named HTLV-II. This virus is associated with a neurologic disease similar to HAM/TSP. It too is a lifelong infection with no effective vaccine and has an even higher prevalence (99%) of asymptomatic patients³.

Retroviruses possess an RNA genome and replicate via a DNA intermediate, which can be integrated into the host's genome and enable the virus to replicate as part of the cell's DNA. Retroviral resistance to antiviral medication is a result of the regular mutations inherent in this process known as reverse transcription.

Transmission and prevention

HTLV-I and HTLV-II share approximately 70% of their genomes but tend to infect different populations. The same rates of infection are seen in endemic populations wherever they migrate.

In Europe, HTLV-I is mainly found among people who have originated from endemic areas: southwestern Japan, the West Indies, Central Africa, the Caribbean basin and southeastern USA. The National Centre for Human Retrovirology estimates that around 22,000 of the UK’s population carry the HTLV-I infection but less than 1,000 are actually aware of their status⁴.

HTLV can be transmitted from mother to baby (particularly via breastfeeding), via unprotected intercourse, blood transfusions and the sharing or re-use of needles and syringes to inject drugs.

Research has shown that transmission routes vary geographically. Localised clustering of infection and social customs suggest the virus is more dependent on mother-to-child transmission in Japan while sexual transmission is more common in the Caribbean.

Prevention measures include safe sexual practices, the use of disposable syringes and blood screening.

1. Dougan et al, New diagnoses of HTLV infection in England and Wales: 2002-2004. Eurosurveillance, 2005; 10(2)
2. Mahieux & Gessain, New human retroviruses: HTLV-3 & 4, Médecine Tropicale, 2005; 65(6)
3. www.htlv1.eu/htlv/htlv_two.html
4. www.htlv1.eu/htlv/htlv_one.html