HIV Vaccine: The race that turned into a marathon

HIV Vaccine: The race that turned into a marathon

Vaccines have been modern society’s most potent weapon against viral diseases. From the worldwide eradication of smallpox back in the 1970s to modern time curbing of the COVID-19 virus, vaccines have saved millions upon millions of lives. [Related article: How Vaccines Work and How You Body Fight Diseases] Usual vaccine development takes years, and yet the COVID-19 pandemic had scientists pushing out vaccines in months. But one virus, the culprit for a worldwide epidemic for the past 40 years, still thwarts those who want to create a vaccine against it– Human Immunodeficiency Virus (HIV).

Acute Immunodeficiency Syndrome (AIDS) is caused by HIV. AIDS/HIV was first discovered in the early 1980s, and as of 2018, 37.9 million people worldwide are infected by HIV. When HIV was first identified in 1984, then U.S. Secretary of Health and Human Services Margaret Heckler announced at the time that they hoped to have a vaccine ready within two years. It’s been 37 years, and the world still does not have an HIV vaccine. 

The history of HIV vaccine development has been marked by numerous setbacks and disappointments. Oftentimes it seems that an unforeseen obstacle sets them back by one and even two steps for every step researchers take forward. It’s so hard to develop an HIV vaccine because it’s different from other types of viruses.


1. Life Cycle
 Lytic cycle vs Lysogenic cycle ©2000 How Stuff Works

Unlike influenza or SAR-coV-2 (the virus that caused the COVID-19 pandemic), which undergoes the lytic cycle, HIV undergoes the lysogenic cycle. Lytic and lysogenic cycles are interchangeable methods of viral multiplication. 

The lytic cycle is relatively more common, wherein a virus infects a host cell, uses its metabolism to multiply, and then destroys the cell completely. On the other hand, the lysogenic cycle is a rarer method of viral reproduction. The virus integrates its genetic information with that of the host and then becomes dormant, letting the host multiply and continue its normal activities. At some point, the virus is triggered, and it thereafter goes on to multiply and ultimately, destroys the host cell. In other words, after an HIV infection, the virus does not reproduce right away. Instead, they mix their genetic instructions into the host cell’s genetic instructions, shielded from the host’s immune system. When the host cell reproduces, the viral genetic instructions get copied into the host cell’s offspring.

2. Genetic variation

Efforts to develop a vaccine against HIV have been hampered by the large genetic diversity of the virus. The replication cycle of HIV is not only very fast (a little over 24 hours) but is also prone to errors. The replication mechanism creates mutated copies of the HIV genetic code, which recombines into new strains when the virus is passed from one person to another. The virus has also evolved to be able to tolerate many mutations in its genetic sequence. With over 60 dominant strains, as well as a multitude of recombinant strains, developing a single vaccine to eradicate the virus seems like an almost impossible mission. Conventional vaccines, like that of SAR-coV-2, only protect a limited number of viral strains.

3. Unique protein coat

HIV has also an incredible ability to shield itself from detection by antibodies in our body. Enveloped viruses such as coronavirus encode a structure on their surface, which is used by viruses to gain entry into a cell. This structure, known as “glycoprotein”, consists of both sugars and proteins. In the case of HIV, its envelope glycoprotein is extreme – it is the most heavily sugared protein of all viruses across all 22 families of viruses. Through natural selection, HIV has figured a way to use these sugars as shields to protect itself from antibodies that the infected host cell makes. The host cell, unfortunately, views these sugars as self and will not elicit a response towards the virus.

4. Immune response

Fighting HIV requires a robust response from the human immune system, but there exists a paradox. Upon detection of a viral infection, specialised white blood cells called CD4 T-cells initiate a defence response by signaling killer cells to the site of infection. This is the same response that will be initiated when a person receives a vaccine. However, these are the very cells that HIV targets for infection. As such, HIV hobbles the body’s ability to defend itself as its CD4 population is depleted systematically. This results in the eventual breakdown of defences, known as immune exhaustion. 

There is still hope. Scientists have come up with new approaches to tackle this virus, some of these treatments are going through clinical trials. We may finally be able to reach. the finishing line after all these years.

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