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March 28 - April 19, 2020
the virus can cross the placenta and infect the foetus causing tissue damage. In addition, the virus has been detected in semen from a proportion of men who have recovered from Zika fever and a few sexually transmitted cases have been recorded.
the cooler months of 2016–17 the Zika epidemics subsided, but by then the virus had increased its range of vector mosquitoes to include non-tropical species. Thus the virus is expected to spread more widely through the Americas, Europe, and Australasia.
As the
Once an acute emerging virus such as a new strain of flu is successfully established in a population, it generally settles into a mode of cyclical epidemics during which many susceptible people are infected and become immune to further attack. When
Viruses spread between hosts in many different ways, but those that cause acute epidemics generally utilize fast and efficient methods, such as the airborne or faecal–oral routes. The former is the most efficient method of spread in industrialized nations where people tend to live in crowded towns
airborne viruses mainly causing respiratory illnesses, like flu, the common cold, or pneumonia,
faecal–oral contamination causing intestinal upsets, with nausea, vomiting, and diarrhoea.
killed around 300 million in the 20th century alone.
Although chickenpox behaves like a classic acute infectious disease analogous to measles, mumps, and rubella, the virus remains in the body for life after the initial infection and may later resurface to cause shingles.
The common cold virus, or rhinovirus, alone has over one hundred different types, and there are many other viruses that infect the cells lining the nose and throat and cause similar symptoms, often with subtle variations.
genuine attack of flu caused by influenza A or B virus is quite a different matter. Although producing similar respiratory symptoms, flu has more severe constitutional effects with additional aching muscles and fever, often lasting for seven days.
three basic manoeuvres: finding a niche in which to hide from immune attack, manipulating immune processes to benefit the virus, and outwitting immune defences by mutating rapidly.
From this early beginning, herpesviruses have co-evolved with their hosts, each partner exerting selective pressure on the other until they have become remarkably well adapted to each other’s lifestyles, allowing the viruses to thrive long term, generally without detriment to the hosts.
To date, over 150 different herpesviruses have been identified, all of which are large, enveloped DNA viruses coding for between 80 and 150 proteins. They are fragile viruses that cannot survive independently for long and so they tend to spread by close contact between infectious and susceptible
Without exception, herpesviruses establish a lifelong infection, often called a latent infection. The viruses survive inside host cells in a dormant state, having shut down their protein production, thereby becoming invisible to host immunity. Occasionally, during the lifetime of the host this latent infection reactivates to produce new viruses.
Table 1. The human herpesviruses—primary infection, prevalence, and site of latency
Eight herdpes viruses chart
HSV infection of the skin soon attracts the attention of immune cells and the lesions heal rapidly, but not before some virus particles have secretly infected nerve endings in the skin and climbed up the nerve fibres to the cell nucleus where they establish latency.
Latent VZV can reactivate to cause shingles at any time in life, but this is most common in the elderly. Reactivation usually occurs in a single nerve cell, causing the typical painful shingles rash of tiny blisters along the course of that particular nerve. As infectious viruses are shed from these lesions, individuals who have not had it before
catch chickenpox from them. But shingles is not caught either from cases of shingles or chickenpox, as it is the result of reactivation of internal, latent viruses.
On rare occasions, EBV causes tumours (see Chapter 8) and has also been suggested as the cause of several other diseases, particularly autoimmune diseases such as rheumatoid arthritis and multiple sclerosis (see Chapter 10).
was the unique occurrence of HIV-1 group M’s spread from Africa to Haiti and on to the USA in the 1960s that prompted the first description of AIDS in 1980 and the isolation of the virus in 1983.
Evidence of declining immunity and the imminent onset of the symptomatic phase of the HIV infection, AIDS, often includes weight loss, night sweats, recurrent chest infections, skin lesions such as warts, and oral ulcers and infections like thrush and cold sores.
To date, five human hepatitis viruses have been discovered and named A, B, C, D, and E.
hepatitis B and C viruses may persist after primary infection, and this can lead to chronic hepatitis, cirrhosis, and liver cancer. Hepatitis D virus (HDV), also known as delta virus,
HCV currently infects around 170 million people. Infection occurs worldwide but shows marked geographical variation, with 1–2 per cent of the population infected in the USA, northern Europe, and Australia, and rates of up to 5 per cent
Only about one-quarter of those with primary HCV infection develop hepatitis with symptoms, but whether symptomatic or not, around 80 per cent of acute HCV cases progress to a chronic phase.
HCV has many ways of dodging the body’s immunity. As an RNA virus, HCV, like HIV, mutates rapidly and this, combined with its extremely high replication rate, generates
HCV also evades host immunity by blocking antiviral mechanisms inside infected cells, preventing the production of cytokines like interferon that might otherwise curtail its spread in the liver. The virus also induces regulatory T cells that paradoxically damp down anti-HCV immunity.
there are signs of ongoing liver damage in all chronic HCV carriers, many of whom are unaware of the infection, and this progresses to chronic active hepatitis and/or cirrhosis in up to 70 per cent of cases.
No vaccine is available to prevent HCV infection, and with 3 per cent of the world’s population currently infected, this is now the commonest cause of liver failure and indication for liver transplantation in the Western world. Chronic
HBV was discovered by chance in 1964 in the blood of an Australian Aborigine and shown to be a major cause of transfusion-associated hepatitis. The virus is extremely infectious and carriers have high viral loads in blood and body fluids. It spreads by close contact, particularly sexual intercourse, and mother to child, as well as by blood contamination of medical instruments, dental drills, and needles used for injection, and household utensils such as razors, toothbrushes, and by tattooing, body piercing, and acupuncture. Intravenous drug users and gay men are at particular risk of
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most healthy adults clear the virus within six months.
Just 1–5 per cent of adult cases lead to lifelong persistence, and this may cause liver damage, cirrhosis, and/or cancer later in life.
Using a combination of tumour-susceptible strains of laboratory animals and cell culture techniques, they identified specific viral genes which could convert, or transform, normal cells into tumour-like cells in a culture dish and also induce them to form tumours in laboratory animals. These genes are called viral oncogenes, and unravelling the various ways in which they transform cells has been instrumental in uncovering the molecular mechanisms involved in cancer development in general. Most
Tumours develop when a single cell in an organism is somehow released from the usual constraints that regulate its growth, and it replicates unchecked.
This rogue cell then produces a mass of similar cells, forming a tumour (or cancer) that invades the surrounding tissues and may spread from its original site.
One in three people develop cancer at some time during their lives, resulting in nearly 11 million new cases, and well over 6 million deaths worldwide every year.
However, the onset of cancer is not an abrupt process resulting from a single cellular event, but a long journey during which the cell undergoes a series of ‘hits’ that induce mutations and eventually turn it into a cancer cell.
tumour is usually a rare and late outcome of infection with a tumour virus.
human tumour viruses discovered are persistent viruses that successfully evade their hosts’ immune attack and remain on board long term. This is a rather comfortable position for a virus to be in, and it is hard to see why it should evolve
tumorigenic properties since killing its host is not advantageous to its survival. But now that the mechanisms involved in viral oncogenesis
sarcoma virus, were mostly RNA retroviruses. Uniquely, when these viruses infect a cell, they produce a DNA copy of their RNA genome, a provirus, which inserts into the cellular genome and thereafter is replicated along with cellular DNA (see Chapter 1). This remarkable feat not only protects the virus from immune attack and ensures its survival for the lifetime of the cell, but also has the potential to reprogramme the cell’s own gene expression, so influencing its growth control mechanisms.
retroviruses. These scientists used the recently identified T cell growth factor called interleukin-2 to grow
HTLV-1 persists in blood T cells for life, but the infection is generally harmless. However, between 2 per cent and 6 per cent of cases progress to ATL or lymphoma, both of which are generally aggressive, difficult to treat, and rapidly fatal.
One particularly important function is the production of a self-stimulatory growth loop that causes the cell to produce the T cell growth factor, interleukin-2. At the same time, it up-regulates the expression of the T cell growth factor’s receptor on the
the eight known human herpesviruses, two are oncogenic—Epstein–Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV).
People whose immune systems are suppressed are also at risk of tumours caused by these viruses because they are incapable of controlling the latent virus infection.
there are five human hepatitis viruses (A, B, C, D, and E), of which hepatitis B and C viruses cause liver cancer.
HBV being a small DNA hepadnavirus, whereas HCV is a flavivirus with an RNA genome.
some people, they persist, often causing continued liver damage, cirrhosis, and, in the unfortunate few, liver cancer.
