How Viruses Reproduce

To understand how viruses reproduce, we need to look at two specific subjects:

The Virus Organism and The Virus Life Cycle


A virus is a small infectious agent that can replicate (reproduce) only inside the living cells of an organism.  Viruses can infect all types of organisms, from animals and plants to bacteria and all forms of living entities – but they CANNOT REPRODUCE BY THEMSELVES!  Viruses require the ability to attach to and insert their viral DNA or RNA into a human host cell in order to reproduce.

Since the discovery in 1898 of the tobacco mosaic virus, about 5,000 viruses have been discovered and described in detail – although there are millions of different types. Viruses are by far the most single abundant biological entities on Earth – far outnumbering all other types of living organisms combined!

Viruses are found wherever there is life and have probably existed since living cells first evolved. Recent discoveries have uncovered that even parts of our human DNA contain remnants of ancient virus DNA!

Virus particles are also known as ‘virions’, and they are typically comprised of only a few components:

First, there is the viral genetic material in the form or either DNA or RNA – long molecules that carry genetic information and the instructions for viral replication.

Next, there is a protein coating that protects these genes – a capsule, envelope, or ‘nucleocapsid’.  In some cases there is an additional layer of lipids that surrounds the protein coat when the virus particles are outside a host cell.

In the Herpes virus (and many other viruses) there is a ‘tegument’, also known as a ‘viral matrix’, lining the space between the nucleocapsid (the inner portion of the virus) and the viral outer envelope, or viral membrane. The tegument is made of proteins which aid in viral DNA replication, as well as helping the virus evade the body’s immune system.

Most viruses (including all the Herpes viruses) have structures around the outside of the viral envelope that are used as attachment points – spike-like structures where the virus particle attaches itself to, and penetrates the membrane of its target host cell.  This is becoming a more and more important element in the fight against viral disease.

The shapes of viruses range from simple spherical, helical and icosahedral forms to more complex structures.  The average virus is about one one-hundredth the size of the average bacterium. Thus, most viruses are much too small to be seen directly with an optical microscope and can only be seen using a special electron microscope, used to visualize very small structures. Viruses are so small that it would take 30,000 to 750,000 of them (depending on the specific virus), laid side by side, to stretch to one centimeter.

A simplified diagram of a typical Herpes simplex virus is shown here:

  1. VIRAL DNA – the genetic material that enables the virus to replicate inside a host cell
  2. NUCLEOCAPSID – the capsule that surrounds and protects the genetic DNA
  3. TEGUMENT – aids in viral DNA replication, and helps the virus evade the body’s immune system
  4. VIRAL ENVELOPE – outer surface of the virus; comprised of glycoproteins to help in the process of attachment to host cells
  5. RECEPTOR / ATTACHMENT SPIKES – specific points where the virus particle attaches to and penetrates the host cell membrane, enabling the virus to insert its VIRAL DNA and begin the replication cycle inside the host cell


Viruses do not reproduce through cell division, because they are ‘acellular’.  Instead, they use the components, mechanisms and metabolic processes of a host cell to produce multiple copies of themselves, and they assemble inside the host cell before the newly formed virus particles are released into the system, each one finding the next host cell to attach to, and repeating the reproduction cycle over and over.

The exact life cycle of viruses differs between species but science agrees that there are six basic stages in the life cycle of viruses:


‘Attachment’ is the first stage in the viral life cycle following introduction of the virus into the body.  It refers to the binding (or attachment) between the proteins that line or surround the viral capsid and specific receptors on the cellular surface of the targeted host cell.

If attachment – also called ‘VIRAL FUSION’ – does not or cannot occur successfully, the viral life cycle is cut short, and the immune system can act to eliminate the attacking virus particle before it has had a chance to penetrate the host cell wall and insert its DNA or RNA.

This mechanism has evolved to favor those viruses that infect only cells within which they are capable of replicating. Thus, specific viruses attach only to specific types of host cells. Attachment to the host cell can result in the fusion of viral and cellular membranes, or changes in the virus surface proteins that allow the virus to enter or penetrate the host cell and begin to replicate.


Following successful attachment to a host cell, the next stage in the viral life cycle is called ‘Penetration’. Viruses enter the host cell through receptor-mediated ‘endocytosis’ (breaching the host cell wall) or membrane fusion. This is often called ‘viral entry’.  Viruses penetrate their host cells through spike-like extensions on the outside envelope of the virus which can puncture the host cell membrane.

Penetration has one singular objective: to insert the viral DNA or RNA inside the host cell, where it can start the process of replication, creating new viral particles. Remember that Penetration cannot occur until Attachment (or Viral Fusion) has been achieved.


Following successful Viral Fusion (Attachment) and having penetrated the host cell wall and inserting its viral DNA or RNA into the host cell, the next stage in the viral life cycle is called ‘Uncoating’.

Uncoating is a process in which the viral capsid is removed: This may be accomplished by degrading the viral envelope with viral enzymes or host cell enzymes, or by simple dissociation of the viral capsule.

The end result, or objective, of Uncoating is the releasing of the viral genomic nucleic acid (the virus’ DNA or RNA), which starts the process of viral replication and reproduction.


‘Replication’ of viruses is exactly what it sounds like: multiplication of the genome – the virus’ DNA or RNA, which are instructions for replicating new viral particles.

In essence, Replication comprises the first steps in creating new viral particles, and preparing them to be ‘Assembled’ into fully functional viruses, capable of attaching to new host cells and starting the cycle over, and so on.


Following the successful replication of the viral genetic structure and the reproduction of the chemicals necessary to create a viral envelope to contain the genetic material of the newly created viruses, self-assembly (‘Viral Assembly’) of the virus particles is then completed, forming a whole new viral particle (think of these as ‘baby viruses’).

This process is sometimes referred to as ‘Maturation’, and is the last step in the viral replication process prior to the newly formed viruses being released into the system where they start the entire life cycle again, commencing with Attachment to a new host cell.


Once newly formed and completed virus particles are fully replicated inside the host cell, they are ready to enter the body’s system and are ‘Released’ to start the life cycle process all over again with Attachment to a new, uninfected host cell.

Viruses can be released from the host cell by lysis, a process that kills the host cell by bursting its membrane and cell wall if present: this is a feature of many viruses. (Think of blowing up a balloon: at a certain point, the balloon cannot hold any more air, and it bursts open; now imagine a human cell exploding with newly formed virus particles.)

Some viruses, which in their completed state have a more substantial envelope coating the virus, may be released from the host cell through a process known as ‘Budding’.

During this process the virus acquires its envelope, which is a modified piece of the host’s plasma or other internal membrane or component of the host cell in which the virus has replicated itself.

It is important to note that viral replication (completion of the entire life cycle) can happen very quickly, and result in the rapid proliferation of new viral particles; in many cases literally millions of newly formed viral particles are created and released into the system.  Thus, the potential for infection (Attachment) of new host cells is quite substantial.

If the life cycle process is prevented, interrupted or interfered with, so that the viruses cannot initially attach to a target host cell, or cannot successfully complete their replication inside the host cell, or are prevented from being assembled or released, the viral life cycle may be cut short or stopped.

Research into all possible approaches to interfere with or impede the viral life cycle are actively being pursued, including drugs which can interfere with viral genetic replication, attempts to create vaccines which may prevent Viral Fusion, and the use of supplements to inhibit Viral Fusion are all key objectives of viral medicine and research.

In reality, there are many opportunities to reduce the likelihood of successful viral life cycle completion, starting with inhibiting the initial Viral Fusion – or Attachment to a host cell – to preventing completion of viral replication.  Given that viruses remain in the body forever, approaches that assist in keeping viruses dormant are also being developed, and may be assisted by various dietary, physical or life-style changes, and by using specific supplements that have been shown to have a damping effect on some stage of the viral life cycle.

Avoiding triggers that may re-awaken dormant viruses is also an important part of maintaining proper health for those infected with various viruses, and specifically for those infected with HSV-1 and / or HSV-2.


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