Kaposi’s sarcoma (KS) is a multifocal tumour only found in a few groups of people, including elderly Mediterranean men, individuals in Africa and patients with immune disorders. The tumours arise from the formation of new blood or lymphatic vessels (angiogenesis or lymphangiogenesis) due to the proliferation of endothelial cells. In 1994 Chang and Moore identified a new virus, Kaposi’s sarcoma-associated herpesvirus (KSHV) as the cause of these tumours.
Unlike other herpesviruses, the seroprevalence of KSHV is not ubiquitous, perhaps only 5% in those countries with low KSHV rates such as the USA and Northern Europe). Like all herpesviruses, KSHV infection persists for the life of the host and can enter either of two states: latency or lytic reactivation. In latency, the minimum number of viral genes is expressed to maintain the virus genome in dividing cells, evading immune detection. Lytic reactivation occurs when the virus re-enters productive replication to generate new progeny, lysing the host cell in the process. And like all herpesviruses KSHV likes to mess with the immune system of its host. The KSHV genome contains 86 genes, almost a quarter of which encode proteins with immunoregulatory activities such as T- and B-cell function, complement activation, the innate antiviral interferon response and natural killer cell activity. Many of these gene are homologues of cellular proteins.
The KSHV proteins MIR1 and MIR2 ubiquitinate the cytoplasmic tail of MHC-I which triggers endocytosis and proteasomal degradation. This protects KSHV-infected cells from NK-mediated lysis. MIR2 can also down-regulate other components of the immune synapse, ICAM (CD54) and PECAM (CD31) by the same mechanism.
The KSHV vOX2 protein causes the cellular CD200 receptor to deliver an inhibitory signal to granulocytes, although the mechanism by which this acts is not yet well defined.
The KCP protein is present on the surface of KSHV virions and infected cells and protects them from complement attack by accelerating the decay of the classical pathway C3 convertase enzyme complex.
The K15 protein activates MAP kinases and this affects immune function.
KSHV encodes a family of 12 miRNAs. These regulate both B- and T-cell function.
The K1 protein reduces the presence of B cell receptors on the surface of B cells and interferes with the production of cytokines, and inhibits apoptosis.
The MIR2 protein down-regulates tetherin, which is involved in normal B-cell differentiation.
Three KSHV chemokine homologues (vCCL1–3) have affinity for chemokine receptors (CCRs) and this affects T-cell responses.
KSHV proteins inhibit interferon pathways.
Since KSHV infection results in lifelong persistence of the virus, these immunomodulation activities are clearly successful in preventing its elimination by the immune system. Many questions about KSHV infection remain unanswered, but we have learned valuable lessons about the normal function of the immune system through studying this virus.
A recent paper in Trends in Microbiology examined the possibilities for using bacteriophages in controlling biofilms which might result in healthcare-associated infections (Preventing biofilms of clinically relevant organisms using bacteriophage. 2009 Trends in Microbiology 17: 66-72). Biofilms are firmly attached microbial communities in which the organisms produce an extracellular polymeric matrix. Biofilm organisms might cause disease by detachment of individual cells or clumps of cells, by production of endotoxin, or by providing a niche for the development of antibiotic-resistant organisms. Biofilm organisms are usually tolerant to antimicrobial agents and the treatment of indwelling medical device-associated infections with systemic antimicrobial agents is usually ineffective.
Bacteriophages have been used for the treatment of infectious diseases in plants and animals, although few clinical trials with stringent negative controls have been carried out. There is a renewed interest in phage therapy in light of growing concerns with antimicrobial resistance in healthcare institutions worldwide. The use of phages for the treatment of device-associated infections could reduce the use of antibiotics and might limit the spread of resistant organisms.
There is some evidence for the potential of phages in biofilm control. Bacteriophage T4 phage was effective against E. coli biofilms in a glucose-limited chemostat, although the rate of phage synthesis and assembly were directly proportional to the amount of protein synthesis in the host cell. Some phages produce polysaccharide depolymerases that have the potential to degrade the biofilm matrix.
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However, there are several important characteristics of phage that should be considered when evaluating the potential of phages to control clinically relevant biofilms. The specificity of receptors for a single phage strain will determine its host range; some phage have specificity at the strain level, such as strain typing phages, whereas some are more broad-spectrum and can infect multiple strains or related species. This high degree of specificity could be a drawback, especially in the case of polymicrobial biofilms.
Few studies have explored the role of biofilms in the development of phage-resistance. Phage cocktails developed via the isolation of host range mutants and broad spectrum phage could be advantageous. Another important question is how a patient’s immune system will respond to the therapeutic introduction of phage. Phages are antigenic and elicit a response by serum antibodies and the cellular immune system. Repeated exposure to the phage results in increasing antibody titers and studies in animal models have shown that phage is cleared from the bloodstream by the cellular immune system. In a short-lived treatment, the antibody response to phage is weak except in cases were serum antibody titers are present before phage treatment. It is possible, although unproven, that phage might associate with biofilms and thereby be protected from inactivation. It might also be possible to design mutant phages with enhanced ability to resist clearance by the cellular immune system.
Measles virus (MV) is one of the most contagious human pathogens. It is transmitted by aerosols, infecting a new host via the upper respiratory tract. Eventually, infection can spread to many organs of the body. The host cell receptors for MV are well defined: CD46, a member of the human complement regulatory proteins and a ubiquitous cellular receptor found on all nucleated cells, and CD150 or SLAM (signalling lymphocyte activation molecule), a membrane glycoprotein present on activated B cells, T cells and monocytes. It is generally believed that laboratory and vaccine strains of MV use both CD150 and CD46 as their cellular receptors, but wild-type MV strains mainly use CD150.
Oncolytic viruses have been selected or engineered to replicate in tumour cells. Approaches towards targeting cancer cells frequently exploit antigens that are unique to or are over expressed on the surface of tumour cells. As cell surface recognition and virus entry is the key first step for specific targeting, engineering oncolytic viruses in order to recognize exclusively the tumour cell-surface is important. Therefore, retargeting of oncolytic viruses a promising approach to exploit the potential of virotherapy.
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Although virotherapy of hard-to-treat tumours with engineered viruses is a tantalizing prospect, this approach is still limited to laboratory studies at present. In order to develop a practical oncolytic treatments, successful tests in vitro using susceptible cells must lead to evaluation of the efficacy of tumour reduction in vivo in animal models with objective measurable parameters of safety and efficacy. Only then will we be ready to begin consideration of human trials of these potent new weapons in the fight against cancer.
It has been estimated that around 2% of the world’s population, approximately 170 million people, are infected with hepatitis C virus (HCV). Over 4 million people in the USA are infected with HCV, a prevalence rate of 1.6%. The peak prevalence of HCV infection occurs among people of 40 to 49 years of age and a history of injection drug use is the strongest risk factor. The UK Health Protection Agency’s annual reports on HCV estimate that in England and Wales around 4,500 people are suffering from severe liver disease due to chronic HCV infection, and that this could rise to around 7,000 by 2010. Over 200,000 UK residents have chronic HCV infection, but five out of six are unaware of this. It is believed that around 80% of UK HCV infections are linked to the use of injected drugs, and 50% of injecting drug users are infected with HCV.
The majority of cases of HCV infection give rise to an acute illness, but up to 80% may then develop into chronic hepatitis. Almost all patients develop a vigorous antibody and cell-mediated immune response which fails to clear the virus infection but may contribute to liver damage. Spontaneous resolution of chronic liver disease is very rare (<2%) and patients with chronic disease are at risk of developing hepatocellular carcinoma (HCC).
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So HCV is a pretty important virus, but it has not been the easiest virus to study. The virus only infects only humans and chimpanzees and effectively cannot be grown in the laboratory. Consequently, until now studies of this virus in animal models have been restricted to chimpanzees and to immunodeficient mice transplanted with human hepatocytes hampering understanding of the virus and drug development. A paper in the most recent edition of Nature identifies a host protein that is essential for HCV entry into cells (Human occludin is a hepatitis C virus entry factor required for infection of mouse cells. Nature 457: 882-886, 12 February 2009). If this protein could be introduced into cells by genetic manipulation, this might produce new models for the study of HCV infection, and manipulating the protein in humans might be a route to protection against the virus.
The newly-identified protein which plays a role in HCV cell entry is occludin (OCLN), a protein involved in forming the tight junctions between cells. The researchers showed that adding this protein to mouse cells makes them susceptible to infection with HCV. Several other HCV cell entry factors had previously been identified, including CD81, scavenger receptor class B type I and claudin-1 (CLDN1). The mouse versions of SR-BI and CLDN1 function at least as well as the human proteins in promoting HCV entry, but OCLN and CD81 must be of human origin to allow efficient infection of mouse cells. The identification of the essential cell entry factors for HCV is an important advance in efforts to develop new models to allow us to study and fight this virus.
Retroviruses have been studied for over 100 years since the discovery by Ellerman and Bang in 1908 that cell-free tissue filtrates could transmit leukaemia in chickens. The first pathogenic human retrovirus (HTLV) was discovered in 1981 and HIV, the causative agent of AIDS was discovered in 1983, but this presentation concentrates on the basic biology of retroviruses.
Retrovirus particles consist of a core, which contains the RNA genome of the virus plus the nucleocapsid (NC) protein and reverse transcriptase (RT), integrase (IN) and protease (PR) enzymes. The core lies inside an icosahedral capsid (CA protein) which is surrounded by the matrix (MA) which links the capsid to the lipid envelope. The transmembrane protein (TM) and surface glycoprotein (SU) are associated with the envelope.
All retrovirus genomes consist of two molecules of RNA, which are equivalent to mRNA. These range in size from ~7-11kb. Retrovirus genomes have four unique features:
They are the only viruses which are fully diploid.
They are the only RNA viruses whose genome is produced by cellular transcriptional machinery (without any participation by a virus-encoded polymerase).
They are the only viruses whose genome requires a specific cellular RNA (tRNA) for replication.
They are the only plus-sense RNA viruses whose genome does not serve directly as mRNA immediately after infection.
The gene order in all retroviruses is the same:
5′ – gag – pol – env – 3′
Some retroviruses have additional genes, such as the tax and rex genes in HTLV and tat and rev in HIV.
To initiate infection, the SU envelope glycoprotein binds to a specific receptor on the surface of the host target cell. The specificity of this interaction does much to determine the cell-tropism of different retroviruses, or even different isolates of the same virus (e.g. in HIV). Receptor binding results in conformational changes in the glycoprotein spike, revealing the (previously masked) fusion domain in the TM protein and resulting in fusion of the virus envelope with the cell membrane. Penetration and uncoating are poorly understood, but it is now known that uncoating is only partial, resulting eventually in a core (nucleocapsid) particle within the cytoplasm. Reverse transcription occurs inside the ordered structure of this core particle. During reverse transcription, the two single-stranded genome RNA molecules are converted into one double-stranded DNA version of the virus genome, which has the addition of long terminal repeats (LTRs).
The double-stranded DNA form of the virus genome is integrated into the chromatin of the host cell by the integrase (IN) enzyme, where it is known as a provirus. Promoter sequences in the upstream LTR direct expression of virus genes using host cell RNA polymerase. Alternative splicing is used to express virus genes gag, pol and env. In addition to encoding the gag proteins, the full length mRNA transcript also forms new genomes which are packaged into virus particles.
The genetics of retroviruses are complex:
High mutation rate – reverse transcription is an error-prone process.
Recombination – occurs during reverse transcription, promoted by the combination of two strands of RNA into one double-stranded DNA provirus.
Interactions with the host cell – insertional mutagenesis, transduction.
In addition to infectious viruses, retrotransposons are endogenous retrovirus-like genetic elements which make up much of the human genome.
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When fish school, birds flock, insects and bacteria swarm, a population of similar individuals cruises along similar, sometimes cyclic, paths. How do the members of a swarm anticipate the movement of others to coordinate movement with them? And how do members, when each is moving rapidly near to others, avoid impeding their neighbor’s motion? These general issues, which have yet to be resolved for any schooling, flocking, or swarming organism, can be investigated in swarming bacteria. Such investigation might have practical value because swarming enables pathogens like Proteus, for example, to invade the urinary tract and to spread along the surface of catheters placed in the urethra. The behavior of swarming individuals might also suggest ways to speed high density automobile or pedestrian traffic and ways to avoid traffic jams. Bacterial sensory systems and behaviors are more amenable to analysis than those of animals. Because they are relatively small; several thousand bacteria can be followed in a time lapse movie of a swarm. Among bacteria that swarm are the hyperflagellated bacteria, all of the Myxobacteria, which lack flagella, and the Bacteriodetes that include Cytophaga, Flavobacteria, and Bacteriodes. Millions of Myxococcus xanthus cells are found to swarm outward for more than a week at a steady rate of approximately 0.1 mm/hr, a rate close to half the speed of individual cell movement. Swarming gives them a significant growth advantage: Whereas cells in the swarmcenter are competing with each other for nutrient and oxygen, cells at the swarm edge have practically unfettered access to both.
Many bacteria can rapidly traverse surfaces from which they are extracting nutrient for growth. They generate flat, spreading colonies, called swarms because they resemble swarms of insects. We seek to understand how members of any dense swarm spread efficiently while being able to perceive and interfere minimally with the motion of others. To this end, we investigate swarms of the myxobacterium, Myxococcus xanthus. Individual M. xanthus cells are elongated; they always move in the direction of their long axis; and they are in constant motion, repeatedly touching each other. Remarkably, they regularly reverse their gliding directions. We have constructed a detailed cell- and behavior-based computational model of M. xanthus swarming that allows the organization of cells to be computed. By using the model, we are able to show that reversals of gliding direction are essential for swarming and that reversals increase the outflow of cells across the edge of the swarm. Cells at the swarm edge gain maximum exposure to nutrient and oxygen. We also find that the reversal period predicted to maximize the outflow of cells is the same (within the errors of measurement) as the period observed in experiments with normal M. xanthus cells. This coincidence suggests that the circuit regulating reversals evolved to its current sensitivity under selection for growth achieved by swarming. Finally, we observe that, with time, reversals increase the cell alignment, and generate clusters of parallel cells.
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Adenoviruses are a frequent cause of acute upper respiratory tract infections, i.e. “colds”. In addition, they also cause a number of other types of infection. They were first isolated in 1953, but in 1962, some adenoviruses were shown to cause tumours in rodents – this caused a considerable panic! However adenovirus oncogenesis appears to be associated with abortive infections and has never been observed in humans. There are at least 51 human adenovirus serotypes which have been divided into subgroups A to F.
Detailed three dimensional structural models of adenovirus particles have been constructed based on a combination of cryoelectron microscopy and X-ray crystallography. There are at least 13 proteins in the adenovirus particle. All adenovirus particles are structurally similar: non-enveloped and 60-90 nm in diameter. They have icosahedral symmetry easily visible in the electron microscope by negative staining and are composed of 252 capsomers: 240 “hexons” + 12 “pentons” at vertices of icosahedron. The pentons have a toxin-like activity, purified pentons causing c.p.e. in the absence of any other virus components. A trimeric fibre protein extends from each of the 12 vertices (attached to the penton base proteins) and is responsible for recognition and binding to the cellular receptor. A globular domain at the end of the adenovirus fiber is responsible for recognition of the cellular receptor.
The adenovirus genome consists of linear, non-segmented, double-stranded DNA, 30-38 kbp long which has the capacity to encode about 40 genes. The terminal sequences of each strand are inverted repeats, hence the denatured single strands can form “panhandle” structures (100-140 bp long). There is a 55kD protein called the terminal protein (TP) covalently attached to the 5′ end of each strand.
The replication of all adenoviruses is similar and occurs in the nucleus of the host cell. Replication is divided into early and late phases, the late phase defined as beginning with the onset of DNA replication. This temporal division is characteristic of the replication of DNA viruses.
Attachment to cells is rather slow, taking several hours to reach a maximum. Uptake of the particle is a two stage process involving an initial interaction of the fibre protein with a range of cellular receptors, which include the MHC class I molecule and the coxsackievirus-adenovirus receptor. The penton base protein then binds to the integrin family of cell surface heterodimers allowing internalization via receptor-mediated endocytosis. Most cells express receptors for the adenovirus fibre coat protein, however internalisation is a more selective process. Penetration involves phagocytosis into phagocytic vacuoles, after which the toxic activity of the pentons is responsible for rupture of the phagocytic membrane and release of the particle into the cytoplasm. Uncoating follows an ordered sequence, first the pentons, releasing a spherical, partially uncoated particle into the cytoplasm. The core migrates to the nucleus where the DNA enters through nuclear pores, where it is converted into a virus DNA-cellular histone complex.
Before and independently of genome replication, immediate early and early mRNAs are transcribed from the input DNA. Transcription of the adenovirus genome is regulated by virus-encoded trans-acting regulatory factors. Products of the immediate early genes regulate expression of the early genes. Early genes are encoded at various locations on both strands of the DNA (l = “leftward strand” and r = “rightward strand”). Multiple protein products are made from each gene by alternative splicing of mRNA transcripts – splicing was first discovered in adenoviruses by Philip Sharp in 1977.
The first mRNA/protein to be made (~1h after infection) is E1A. This protein is a trans-acting transcriptional regulatory factor which is necessary for transcriptional activation of early genes. The protein is also capable of activating transcription from a variety of other virus and cellular promoters and shows no sequence-specificity, rather it causes a modification of the cellular environment. The second protein made is E1B. E1A and E1B together (and independently of other virus proteins) are capable of transforming primary cells in vitro (especially in Ad5, Ad12).
Adenovirus DNA replication has been studied extensively. At least three virus-encoded proteins are known to be involved in DNA replication:
TP – acts as a primer for initiation of synthesis
Ad DBP – a DNA-binding protein
Ad DNA Pol – 140kD DNA-dependent polymerase
In addition, many cellular proteins in the nucleus also participate in replication of the genome (e.g. NFI, NFII, topoisomerase I). The adenovirus genome has inverted terminal repeats (ITRs) of about 100 bp. Located within the ITRs are the cis-acting DNA sequences which define ori, the origin of DNA replication. Covalently attached to each 5′ end is a terminal protein (TP) which is an additional cis-acting component of ori.
At the onset of DNA replication, the pattern of transcription changes radically from the early to the late genes. Late phase transcription is driven primarily by the major late promoter. Although transcription from this promoter is complex involving multiple polyadenylation signals and an elaborate usage of RNA splicing, five gene clusters can be defined (L1-L5). Late phase gene expression is primarily concerned with the synthesis of virion proteins.
Particle assembly occurs in the nucleus, but begins in the cytoplasm when individual monomers form into hexon and penton capsomers. Empty, immature capsids are assembled from these protomers in the nucleus, where the core is formed from genomic DNA plus its associated core proteins.
Certain types of adenovirus are commonly associated with particular clinical syndromes. This list includes relatively common infections (at the top) and some rare infections (at the bottom). Most adenovirus infections involve either the respiratory or gastrointestinal tracts or the eye. Adenovirus infections are very common, most are asymptomatic. Most people have been infected with at least 1 type at age 15. Virus can be isolated from the majority of tonsils/adenoids surgically removed, indicating latent infections. It is not known how long the virus can persist in the body, or whether it is capable of reactivation after long periods, causing disease (it is hard to isolate this occult virus as it may be present in only a few cells). It is known that virus is reactivated during immunosuppression, e.g. in AIDS and transplant patients.
A characteristic feature of adenoviruses is their ability to subvert the host immune response by using the early E3 cassette of genes. The E3 membrane proteins are able to downregulate critical recognition structures for the host immune system from the cell surface.
There is no treatment available for adenovirus infections. Inactivated vaccines have been developed and are routinely used for military recruits in some countries (notably the USA). This is because adolescents and others in close daily contact are at risk for epidemic spread of respiratory infections, but the risk to general population is so low that vaccination is not a viable proposition.
In recent years, there has been considerable interest in developing adenoviruses as defective vectors to carry and express foreign genes for therapeutic purposes. One reason for this is that the adenovirus genome is relatively easily manipulated in vitro (c.f. retroviruses) and the genes coupled to the late promoter are efficiently expressed in large amounts. Adenoviruses have been studied intensively for over 50 years as models of virus-cell interactions and more recently as gene vectors.
Sleep quality is thought to be an important predictor of immunity and, in turn, susceptibility to the common cold. A new article examines whether sleep duration and efficiency in the weeks preceding virus exposure are associated with cold susceptibility. A total of 153 healthy men and women (age range, 21-55 years) volunteered to participate in the study. For 14 consecutive days, they reported their sleep duration and sleep efficiency (percentage of time in bed actually asleep) for the previous night and whether they felt rested. Average scores for each sleep variable were calculated over the 14-day baseline. Subsequently, participants were quarantined, administered nasal drops containing a rhinovirus, and monitored for the development of a clinical cold (infection in the presence of objective signs of illness) on the day before and for 5 days after exposure.
Results: There was a graded association with average sleep duration: participants with less than 7 hours of sleep were 2.94 times more likely to develop a cold than those with 8 hours or more of sleep. The association with sleep efficiency was also graded: participants with less than 92% efficiency were 5.50 times more likely to develop a cold than those with 98% or more efficiency. These relationships could not be explained by differences in prechallenge virus-specific antibody titers, demographics, season of the year, body mass, socioeconomic status, psychological variables, or health practices. The percentage of days feeling rested was not associated with colds.
Conclusion: Poorer sleep efficiency and shorter sleep duration in the weeks preceding exposure to a rhinovirus were associated with lower resistance to illness.
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I recently spent some time as a patient on a ward in an NHS hospital where I had been admitted for some tests. Thankfully, all the results were negative and I was diagnosed as being quite healthy for a person of my advanced age :-)
As anyone who has ever spent any time as an NHS patient knows only too well, one of the defining features of the experience is an awful lot of waiting around. I spent just under a day on a Clinical Decisions Unit ward where patients are admitted for testing and then either discharged or moved on to longer stay wards for treatment. There were a lot of very sick people on the ward, but I was feeling fine, so there wasn’t much I could do other than sit and observe the goings on, which is how I discovered that
Infection control in hospitals is broken
“Hospital superbugs” such as Staphylococcus aureus MRSA, Clostridium difficile and Noroviruses feature prominently in the news media and consequently on MicrobiologyBytes, with claim and counterclaim about increasing, static or declining infection rates constantly being batted backwards and forwards, and the Department of Health publishes endless guidance on infection control procedures. Apart from quack claims of miracle cures, the formal response to hospital-acquired infections are procedures for infection control such as cleaning, disinfection and sterilization, protective equipment and surveillance of infection rates. As an observer on a busy ward I was able to watch what happened as patients and staff came and went.
The care I received was exemplary, and for the most part, the ancillary, nursing and medical staff worked hard and clearly cared about the welfare of the patients. But that’s not enough. The reality is that the complexity of the system pushed all the staff beyond their limits, and damaged morale. As a simple example, I watched a domestic ancillary employed as bed maker drifting around looking for beds to make. She was once about to make one when she was called away, and when she came back, the nurses had made the bed. I listened to the nurses grumble about how the ancillaries didn’t do their jobs properly, and the ancillaries grumble about the nurses. And of course, everyone grumbled about the medical staff. Morale was at a low ebb. But it gets worse. Time and time again I watched ward staff strip the linen from beds which had been vacated by patients and painstakingly disinfect the mattress and the bed before remaking the bed with fresh linen. What’s wrong with that? No-one cleaned the bedside chairs. When the next patient arrived, they kicked their bags around on the floor for a while before putting them on the chair, which the nurses dumped the fresh linen on before making the beds.
In less than 24 hours, I was treated by dozens of medical staff and wheeled all over the hospital for various tests. The ward was like a motorway, with staff, patients and visitors constantly moving from ward to ward, street to common areas, canteens and homes. Flawed understanding of basic microbiology is not compensated for by mandated infection control procedures rigidly-applied without any thought or appreciation. Errors are compounded by a totemic belief in the miracle properties of alcohol hand rubs which adorn every bed but which distract from more effective handwashing procedures. Did I need to be visited by the person flitting from ward to ward to fiddle with the TV/radio/phone console above every bed? Even if they did spend several seconds squirting alcohol gel on their hands before moving on to the next patient? I don’t think so.
Infection control in hospitals is broken by the complexity of the system
So how can you fix it? Apart from better microbiology training, the system needs to be radically simplified so that staff and patients are not constantly moving around. Wards should be much more autonomous with a limited number of staff responsible for them, and allowed to do their jobs properly. This would allow much better standards of care arising from the evident motivation they have. There’s no need for people to flit constantly from ward to ward, delivering meals, borrowing equipment, chasing test results and spreading contamination. Simplify. Let people do the jobs they have been trained for and to feel pride in themselves. Back to basics.
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Kaposi’s sarcoma (KS) is a multifocal tumour only found in a few groups of people, including elderly Mediterranean men, individuals in Africa and patients with immune disorders. The tumours arise from the formation of new blood or lymphatic vessels (angiogenesis or lymphangiogenesis) due to the proliferation of endothelial cells. In 1994 Chang and Moore identified a new virus, Kaposi’s sarcoma-associated herpesvirus (KSHV) as the cause of these tumours.
