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Antiviral drugs are medications used to treat viral infections. Because viruses replicate entirely inside host cells using the host’s machinery, it is difficult to develop drugs that affect viruses without also harming the host. Antiviral drugs do not inactivate or kill viruses, they merely inhibit viral reproduction by interfering with a certain stage of the virus life cycle.
A virus is composed of a genome, DNA or RNA, wrapped inside a protective protein coat, called a capsid. Most animal viruses also have an additional lipid membrane, called an envelope, with protein spikes that serve to attach to host cells.
A viral life cycle typically consists of the following steps:
– attachment to host cell receptor, followed by viral entry: via endocytosis, membrane fusion, or both.
– release of viral genome, also known as uncoating,
– replication of viral genome,
– synthesis and processing of viral proteins, assembly of viral components into new viruses,
– and release of new viruses from host cell.
Antiviral strategies aim to block viral reproduction at any of these stages.
To prevent viral attachment, a drug can either bind to host cell receptor/coreceptor, or to the viral spike protein. Examples are HIV drugs – CCR5-antagonists. They bind to CCR5 coreceptor, masking its binding site for HIV.
For enveloped viruses, one strategy is to prevent fusion of viral and host cell membrane. An agent can bind directly to the viral protein that is responsible for fusion, or disrupt the condition that is required for fusion.
Several drugs have been developed to inhibit the uncoating of influenza A virus – they impair the function of the protein responsible for viral genome release from endosomes.
Viruses that use reverse transcriptase for replication are usually targeted for this enzyme. Because the process of reverse transcription, converting RNA to DNA, occurs only in these viruses and not human cells, drugs targeting reverse transcriptase are generally safe for humans. Most of these agents are nucleoside or nucleotide analogs. They compete with regular nucleotides, insert themselves into the growing chain of DNA, and stop the process prematurely. There are also non-nucleoside reverse transcriptase inhibitors, which bind non-competitively to the reverse transcriptase, impairing its function. The 2 classes of inhibitors are usually combined for maximum effects.
Retroviruses, such as HIV, use viral enzyme integrase to insert their genome into host cell DNA, a critical step for viral reproduction. Drugs that inhibit integrase have been developed to treat HIV and other retroviruses.
Viruses with large DNA genomes usually encode their own DNA polymerase for DNA replication. Viral DNA polymerases are the target of many currently available antiviral drugs. Most of these drugs are nucleoside analogs, they incorporate into the growing DNA and cause premature termination of viral DNA synthesis.
Another approach is to inhibit viral protein synthesis by antisense mechanism. Antisense antiviral drugs are short synthetic nucleic acid strands that are complementary to part of an essential viral mRNA. They bind specifically to the viral mRNA, effectively preventing it from being translated into protein.
Some viruses require activity of a specific protease to cleave precursor viral proteins into functional components for viral assembly. Several drugs have been developed to target this protease in HIV.
Influenza virus requires action of viral enzyme neuraminidase to release new viruses from host cell. Blocking neuraminidase is an effective way to treat influenza.

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Bacterial infections are treated with antibiotics. Antibiotic resistance occurs when an infection responds poorly to an antibiotic that once could treat it successfully. It’s the bacteria that have become resistant to the antibiotic, not the patient. This happens because the bacteria acquire a mutation – a change in their DNA – that gives them a new protein as a tool to fight the antibiotic. There are many mechanisms by which this tool may work. It can:

– prevent the antibiotic from entering the bacterial cell;

– pump the antibiotic out of the cell;

– destroy the antibiotic by enzymatic reaction;

– modify the antibiotic’s target so it no longer binds to the drug;

– or give the cell a way to bypass the antibiotic’s target, making the drug irrelevant.

Mutations in bacterial genome occur all the time, spontaneously, but only the ones that confer a certain advantage would persist to the next generation. Let’s consider a situation when a new mutation emerges and makes the bacteria resistant to a certain antibiotic. In the absence of the antibiotic, such mutation offers no advantage, and because mutations usually come with slower growth, the mutation would be diluted and eventually disappear in the following generations. On the other hand, in the presence of the antibiotic, only bacteria that carry such mutation would survive and they would soon take over the whole bacterial population. The use of antibiotic is therefore the factor that drives the selection of antibiotic-resistant organisms.

Mutations that confer antibiotic resistance can be transmitted not only vertically, from parent cells to offspring, but also horizontally, from one bacterial cell to another, using mobile genetic elements such as plasmids or bacteriophages. This means a bacterial strain can share their antibiotic resistance with other bacterial strains and even with distantly related bacterial species. Horizontal transfer is a major mechanism underlying the spread of antibiotic resistance among bacterial species. These antibiotic-resistant bacteria can infect humans, animals and spread between them through food and the environment.

Antibiotic resistance is one of the biggest global health concerns. Infections by antibiotic-resistant bacteria are much harder, sometimes impossible, to treat. Some bacteria, called superbugs, are resistant to most of the common antibiotics, and are especially difficult to kill. Treatments for infections caused by such bacteria are costly and toxic to the patients.

While the emergence of antibiotic resistance is inevitable, the process is greatly accelerated by misuse and overuse of antibiotics. To help control spread of antibiotic resistance, antibiotics must be taken correctly, only when prescribed by a healthcare professional, who should do so only when antibiotics are needed, according to current guidelines. Antibiotics should not be used to promote growth or prevent diseases in healthy animals. Measures that help prevent infections also help reduce antibiotic overuse.

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Antibiotics are medications used to fight bacterial infections. Originally, the term “antibiotics” referred to natural compounds produced by certain microorganisms for the purpose of fending off others; for example, penicillin is produced by the fungus Penicillium. Nowadays, this term includes all antibacterial products, most of which are semi-synthetic, meaning they are modifications of natural products. Antibiotics are just one type of antimicrobials. They target bacteria, and are usually not effective against other types of organisms. Antibiotics cannot treat viral infections such as common cold or flu.
Antibiotics can be bactericidal, meaning they destroy bacterial cells; or bacteriostatic, meaning they inhibit bacterial growth.
Some antibiotics are broad-spectrum – they are effective against a wide range of bacteria, including both Gram-positive and Gram-negative; while others are narrow-spectrum – they are more specific, affecting a smaller group of bacteria.
Antibiotics can be classified by their mechanisms of action:
– Inhibitors of cell wall synthesis. Bacterial cells are surrounded by cell walls made of peptidoglycan. Antibiotics that affect bacterial cell wall act at different stages of peptidoglycan synthesis and cell wall assembly. Because mammalian cells do not have cell walls, this class of antibiotics is highly selective – they target bacteria and have minimal effects on mammalian host cells.
– Disruptors of cell membrane. Some antibiotics disrupt the integrity of cell membrane by binding to membrane phospholipids. Because cell membrane is also found in mammalian cells, these antibiotics are also toxic to host cells if administered systemically. Their clinical use is therefore limited to topical applications.
– Inhibitors of protein synthesis. Antibiotics that interfere with bacterial protein synthesis may act at different steps of this process, including: formation of the 30S initiation complex, assembly of the 50S ribosome subunit, formation of the 70S ribosome from the 30S and 50S complexes, and elongation process. Some of these antibiotics also inhibit the eukaryotic mammalian counterparts, but their effect on bacterial ribosomes is significantly greater.
– Inhibitors of nucleic acid synthesis. Some antibiotics interfere with DNA synthesis by binding to bacterial topoisomerase II – the enzyme that relaxes the supercoil DNA before its replication. Some others interfere with RNA synthesis by inhibiting RNA polymerase. Some antibiotics of this class are selective – they do not interact with mammalian counterparts of these enzymes, while others do affect mammalian host cells. The latter are used for cancer treatment instead. Because cancer cells grow faster than normal cells, they are more affected by the action of these agents.
– Inhibitors of folic acid synthesis. Bacteria synthesize their own folic acid, unlike humans who get the vitamin from food. Because of this, antibiotics that inhibit enzymes involved in folic acid synthesis only harm bacterial cells, and not human cells.

Feb 2016, WHO has declared the Zika virus a global public health emergency.  What you should know?
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Zika virus is a member of the Flavivirus genus which also includes viruses that cause dengue fever, yellow fever and Japanese encephalitis. The name Zika came from the Zika forest of Uganda, where the virus was first isolated in 1947.

Transmission

The virus is mainly spread through daytime active Aedes mosquitoes, but can also be transmitted by blood transfusion, via sexual contact, and from an infected mother to the fetus during pregnancy.

Zika Fever – Symptoms 

Infection with Zika virus is known as Zika fever. Most infected people, however, do not develop any symptoms. In those who do, the symptoms are usually mild and may include: fever, rash, conjunctivitis, joint pain and headache. The disease commonly clears up on its own after a week and does not require any treatment other than rest.

So why the big fuss?

Originally considered a mild disease, Zika fever has been getting a lot of attention lately due to reported connection between the virus and incidents of microcephaly in infants born from infected mothers.

Microcephaly is a serious birth defect where the brain of the newborn is underdeveloped and so smaller than usual. Depending on the extent of the defect, microcephaly may result in a number of neurological disorders, including: seizures, developmental delay, intellectual disabilities, vision and hearing loss. The problems are usually life-long and may also be life-threatening.

Several studies newly published in May 2016 showed that Zika virus in infected pregnant mice can cross the placenta to the fetuses, where it destroys neural progenitor cells. Because neural progenitors cells are fast-replicating and give rise to a large number of brain cells, even a small loss of these cells would result in missing parts of the brain.

The number of infants born with microcephaly has surged 20 folds in the affected areas of the Brazil outbreak, which started in May 2015. While the link between Zika and microcephaly has not been fully proven, the evidence has become overwhelming.

Infection in adults has also been linked to Guillain–Barré Syndrome, a rare condition characterized by a rapid onset of muscle weakness.

Where is ZIKA now?

Since the start of its outbreak in Brazil, Zika has spread rapidly to other surrounding countries. The World Health Organization warned that the virus is likely to spread to nearly all countries of the Americas, except perhaps Canada and continental Chile, where it is too cold for Aedes mosquitoes to survive. Large outbreaks may also be expected in Asia.

More than a hundred of pregnant women in the US has been tested positive for Zika (May 2016)

The Asian strain that causes Brazil outbreak is now found in Africa

Prevention

There is currently no vaccine for Zika; the best way to prevent the disease is to avoid mosquitoes. Pregnant women are advised not to travel to affected areas and women living in affected countries to delay getting pregnant.